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Hoost SS, Honig LS, Kang MS, Bahl A, Lee AJ, Sanchez D, Reyes-Dumeyer D, Lantigua RA, Dage JL, Brickman AM, Manly JJ, Mayeux R, Gu Y. Association of dietary fatty acids with longitudinal change in plasma-based biomarkers of Alzheimer's disease. J Prev Alzheimers Dis 2025; 12:100117. [PMID: 40107919 PMCID: PMC12094269 DOI: 10.1016/j.tjpad.2025.100117] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/22/2024] [Revised: 01/29/2025] [Accepted: 02/27/2025] [Indexed: 03/22/2025]
Abstract
BACKGROUND Elevated intake of omega-3 polyunsaturated fatty acids is linked to a reduced risk of dementia in some prospective studies. However, few studies have examined the relationship between nutrient intake and plasma biomarkers of Alzheimer's disease. OBJECTIVES We explored whether omega-3, omega-6, and monounsaturated fat intakes were associated with changes in plasma biomarkers of Alzheimer's disease over time. DESIGN The Washington Heights-Inwood Columbia Aging Project is a prospective cohort study (1994-2021); the data set used here includes a mean follow-up of 7.0 years. SETTING Community-based in New York City. PARTICIPANTS 599 dementia-free individuals at baseline who completed a 61-item food frequency questionnaire and had biomarkers measured in plasma from at least two different time points. MEASUREMENTS Fatty acid intake tertiles were computed from participant-completed 61-item Willett semi-quantitative food frequency questionnaires (Channing Laboratory, Cambridge, Massachusetts) obtained once at their baseline visit. Plasma-based biomarker assays were performed, using the single molecule array technology Quanterix Simoa HD-X platform, at baseline and follow-up visits. Generalized Estimating Equations (GEE) models were used to evaluate the association between baseline nutrient intake tertile and changes in biomarkers including phospho-tau181, amyloid-beta 42/40 ratio, phospho-tau181/amyloid-beta42 ratio, glial fibrillary acidic protein, neurofilament light chain, and two biomarker patterns derived from Principal Component Analysis (PCA1 and PCA2), with higher scores indicating a high level of neurodegeneration and low level of Alzheimer's disease burden, respectively). Models were adjusted for age, sex, race/ethnicity, education, and calculated total energy intake initially, and additionally for cerebrovascular risk factors. RESULTS Higher baseline omega-3 intake tertile was associated with lesser decline in PCA2 (β = 0.221, p < 0.001) and amyloid-beta 42/40 ratio (β = 0.022, p = 0.003), and a lesser rise in phospho-tau181 (β = -0.037, p = 0.001). Higher omega-6 intake tertile was linked to a lesser rise in phospho-tau181 (β = -0.050, p < 0.001) and glial fibrillary acidic protein (β = -0.028, p = 0.002). Most associations persisted after adjusting for cardiovascular risk factors. CONCLUSIONS Higher relative baseline intake of omega-3 and omega-6 fatty acids is associated with lesser progression of blood-based biomarkers of Alzheimer's disease. Consuming healthy fatty acids may help prevent accumulation of Alzheimer's disease-related pathological changes.
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Affiliation(s)
- Serena S Hoost
- Department of Neurology, Vagelos College of Physicians and Surgeons, Columbia University, and the New York Presbyterian Hospital, 710 West 168th Street, New York, New York, 10032, USA
| | - Lawrence S Honig
- Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Vagelos College of Physicians and Surgeons, Columbia University, 630 West 168th Street, New York, NY, 10032, USA; G.H. Sergievsky Center, Vagelos College of Physicians and Surgeons, Columbia University, 630 West 168th Street, New York, New York, 10032, USA; Department of Neurology, Vagelos College of Physicians and Surgeons, Columbia University, and the New York Presbyterian Hospital, 710 West 168th Street, New York, New York, 10032, USA
| | - Min Suk Kang
- Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Vagelos College of Physicians and Surgeons, Columbia University, 630 West 168th Street, New York, NY, 10032, USA; Department of Neurology, Vagelos College of Physicians and Surgeons, Columbia University, and the New York Presbyterian Hospital, 710 West 168th Street, New York, New York, 10032, USA
| | - Aanya Bahl
- Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Vagelos College of Physicians and Surgeons, Columbia University, 630 West 168th Street, New York, NY, 10032, USA
| | - Annie J Lee
- Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Vagelos College of Physicians and Surgeons, Columbia University, 630 West 168th Street, New York, NY, 10032, USA; Department of Neurology, Vagelos College of Physicians and Surgeons, Columbia University, and the New York Presbyterian Hospital, 710 West 168th Street, New York, New York, 10032, USA
| | - Danurys Sanchez
- Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Vagelos College of Physicians and Surgeons, Columbia University, 630 West 168th Street, New York, NY, 10032, USA; Department of Neurology, Vagelos College of Physicians and Surgeons, Columbia University, and the New York Presbyterian Hospital, 710 West 168th Street, New York, New York, 10032, USA
| | - Dolly Reyes-Dumeyer
- Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Vagelos College of Physicians and Surgeons, Columbia University, 630 West 168th Street, New York, NY, 10032, USA; Department of Neurology, Vagelos College of Physicians and Surgeons, Columbia University, and the New York Presbyterian Hospital, 710 West 168th Street, New York, New York, 10032, USA
| | - Rafael A Lantigua
- Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Vagelos College of Physicians and Surgeons, Columbia University, 630 West 168th Street, New York, NY, 10032, USA; Department of Medicine, Vagelos College of Physicians and Surgeons, Columbia University, and the New York Presbyterian Hospital, 630 West 168th Street, New York, New York, 10032, USA
| | - Jeffrey L Dage
- Stark Neurosciences Research Institute, Suite 414, Indiana University School of Medicine, 320 West 15th Street, Indianapolis, Indiana, 46202, USA
| | - Adam M Brickman
- Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Vagelos College of Physicians and Surgeons, Columbia University, 630 West 168th Street, New York, NY, 10032, USA; G.H. Sergievsky Center, Vagelos College of Physicians and Surgeons, Columbia University, 630 West 168th Street, New York, New York, 10032, USA; Department of Neurology, Vagelos College of Physicians and Surgeons, Columbia University, and the New York Presbyterian Hospital, 710 West 168th Street, New York, New York, 10032, USA
| | - Jennifer J Manly
- Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Vagelos College of Physicians and Surgeons, Columbia University, 630 West 168th Street, New York, NY, 10032, USA; G.H. Sergievsky Center, Vagelos College of Physicians and Surgeons, Columbia University, 630 West 168th Street, New York, New York, 10032, USA; Department of Neurology, Vagelos College of Physicians and Surgeons, Columbia University, and the New York Presbyterian Hospital, 710 West 168th Street, New York, New York, 10032, USA
| | - Richard Mayeux
- Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Vagelos College of Physicians and Surgeons, Columbia University, 630 West 168th Street, New York, NY, 10032, USA; G.H. Sergievsky Center, Vagelos College of Physicians and Surgeons, Columbia University, 630 West 168th Street, New York, New York, 10032, USA; Department of Neurology, Vagelos College of Physicians and Surgeons, Columbia University, and the New York Presbyterian Hospital, 710 West 168th Street, New York, New York, 10032, USA; Department of Epidemiology, Mailman School of Public Health, Columbia University, 722 West 168th Street, New York, New York, 10032, USA
| | - Yian Gu
- Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Vagelos College of Physicians and Surgeons, Columbia University, 630 West 168th Street, New York, NY, 10032, USA; G.H. Sergievsky Center, Vagelos College of Physicians and Surgeons, Columbia University, 630 West 168th Street, New York, New York, 10032, USA; Department of Neurology, Vagelos College of Physicians and Surgeons, Columbia University, and the New York Presbyterian Hospital, 710 West 168th Street, New York, New York, 10032, USA; Department of Epidemiology, Mailman School of Public Health, Columbia University, 722 West 168th Street, New York, New York, 10032, USA.
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Diener C, Holscher HD, Filek K, Corbin KD, Moissl-Eichinger C, Gibbons SM. Metagenomic estimation of dietary intake from human stool. Nat Metab 2025; 7:617-630. [PMID: 39966520 PMCID: PMC11949708 DOI: 10.1038/s42255-025-01220-1] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 02/14/2024] [Accepted: 01/16/2025] [Indexed: 02/20/2025]
Abstract
Dietary intake is tightly coupled to gut microbiota composition, human metabolism and the incidence of virtually all major chronic diseases. Dietary and nutrient intake are usually assessed using self-reporting methods, including dietary questionnaires and food records, which suffer from reporting biases and require strong compliance from study participants. Here, we present Metagenomic Estimation of Dietary Intake (MEDI): a method for quantifying food-derived DNA in human faecal metagenomes. We show that DNA-containing food components can be reliably detected in stool-derived metagenomic data, even when present at low abundances (more than ten reads). We show how MEDI dietary intake profiles can be converted into detailed metabolic representations of nutrient intake. MEDI identifies the onset of solid food consumption in infants, shows significant agreement with food frequency questionnaire responses in an adult population and shows agreement with food and nutrient intake in two controlled-feeding studies. Finally, we identify specific dietary features associated with metabolic syndrome in a large clinical cohort without dietary records, providing a proof-of-concept for detailed tracking of individual-specific, health-relevant dietary patterns without the need for questionnaires.
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Affiliation(s)
- Christian Diener
- Diagnostic and Research Institute of Hygiene, Microbiology and Environmental Medicine, Medical University of Graz, Graz, Austria.
- Institute for Systems Biology, Seattle, WA, USA.
| | - Hannah D Holscher
- Department of Food Science and Human Nutrition, University of Illinois Urbana-Champaign, Urbana, IL, USA
| | - Klara Filek
- Diagnostic and Research Institute of Hygiene, Microbiology and Environmental Medicine, Medical University of Graz, Graz, Austria
| | - Karen D Corbin
- AdventHealth Translational Research Institute, Orlando, FL, USA
| | - Christine Moissl-Eichinger
- Diagnostic and Research Institute of Hygiene, Microbiology and Environmental Medicine, Medical University of Graz, Graz, Austria
- BioTechMed Graz, Graz, Austria
| | - Sean M Gibbons
- Institute for Systems Biology, Seattle, WA, USA.
- Department of Bioengineering, University of Washington, Seattle, WA, USA.
- Department of Genome Sciences, University of Washington, Seattle, WA, USA.
- eScience Institute, University of Washington, Seattle, WA, USA.
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Wang LY, Hu H, Sheng ZH, Hu HY, Zhang ZH, Tan L. Associations among healthy lifestyle characteristics, neuroinflammation, and cerebrospinal fluid core biomarkers of Alzheimer's disease in cognitively intact adults: The CABLE study. J Alzheimers Dis 2024; 102:855-865. [PMID: 39558781 DOI: 10.1177/13872877241291969] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/20/2024]
Abstract
BACKGROUND The occurrence of Alzheimer's disease (AD) can be partially prevented through healthy lifestyles, but the mechanisms associated with AD pathology are unclear. OBJECTIVE To explore associations among healthy lifestyle characteristics (HLCs), cerebrospinal fluid (CSF) soluble TREM2 (sTREM2), and AD biomarkers. METHODS From the Chinese Alzheimer's Biomarker and LifestylE (CABLE) study, 924 cognitively normal participants were enrolled in this cross-sectional analysis. We defined the following 11 HLCs: appropriate frequencies of coffee and tea consumption, sufficient frequencies of fish and fruit intake, non-social isolation, adequate sleep, regular physical activity, no depression, never smoking, non-hazardous drinking, and well-maintained blood pressure. We categorized participants according to the number of HLCs reported by participants into favorable, intermediate, and unfavorable lifestyle groups. Multiple linear regression was used to investigate the relationship among HLCs, CSF sTREM2, and AD biomarkers. Mediation effects were tested using a causal mediation analysis having 10,000 bootstrap iterations. RESULTS Included subjects were with a mean age of 61.8 ± 10.2 years, of which 41.8% were female. Sufficient fish intake (β = -0.164, p = 0.017) and well-maintained blood pressure (β = -0.232, p = 0.006) were significantly correlated with lower CSF sTREM2 levels. A larger number of HLCs were associated with lower CSF T-tau (p = 0.001), P-tau (p = 0.012), and sTREM2 (p = 0.040) levels. CSF sTREM2 partially mediated the association between the number of HLCs and CSF tau pathology (mediating proportion T-tau: 22.4%; P-tau: 25.0%). CONCLUSIONS HLCs might impact the pathological processes of AD by regulating neuroinflammation.
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Affiliation(s)
- Lan-Yang Wang
- Department of Neurology, Qingdao Municipal Hospital, Nanjing Medical University, Nanjing, China
| | - Hao Hu
- Department of Neurology, Qingdao Municipal Hospital, Qingdao University, Qingdao, China
| | - Ze-Hu Sheng
- Department of Neurology, Qingdao Municipal Hospital, Qingdao University, Qingdao, China
| | - He-Ying Hu
- Department of Neurology, Qingdao Municipal Hospital, Qingdao University, Qingdao, China
| | - Zi-Hao Zhang
- Department of Neurology, Qingdao Municipal Hospital, Qingdao University, Qingdao, China
| | - Lan Tan
- Department of Neurology, Qingdao Municipal Hospital, Nanjing Medical University, Nanjing, China
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Kelebie MA, Tinsae T, Alemayehu BF, Walelign GK, Takelle GM. Prevalence and associated factors of neurocognitive disorder among people living with HIV/AIDS in the South Gondar zone primary hospitals, North-West Ethiopia: an institution-based cross-sectional study. BMJ Open 2024; 14:e082773. [PMID: 38697760 PMCID: PMC11086442 DOI: 10.1136/bmjopen-2023-082773] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 12/03/2023] [Accepted: 04/08/2024] [Indexed: 05/05/2024] Open
Abstract
OBJECTIVE To assess the prevalence and associated factors of neurocognitive disorder among people living with HIV/AIDS in South Gondar primary hospitals, North-West Ethiopia, 2023. DESIGN Institution-based cross-sectional study design. SETTING South Gondar primary hospitals, North-West Ethiopia. PARTICIPANTS 608 participants were recruited using the systematic random sampling technique. MEASUREMENT Data were collected using an interviewer-administered questionnaire and medical chart reviews. The International HIV Dementia Scale was used to screen for neurocognitive disorder. The data were entered through EPI-DATA V.4.6 and exported to SPSS V.21 statistical software for analysis. In the bivariable logistic regression analyses, variables with a value of p<0.25 were entered into a multivariable logistic regression analysis to identify factors independently associated with neurocognitive disorder. Statistical significance was declared at a value of p<0.05. RESULTS The prevalence of neurocognitive disorder among HIV-positive participants was 39.1%. In multivariable logistic regression, lower level of education (adjusted OR (AOR)=2.94; 95% CI 1.29 to 6.82), unemployment (AOR=2.74; 95% CI 1.29 to 6.84) and comorbid medical illness (AOR=1.80; 95% CI 1.03 to 3.14) were significantly associated with neurocognitive disorder. CONCLUSION HIV-associated neurocognitive problems affected over a third of the participants. According to the current study, comorbid medical conditions, unemployment and low educational attainment are associated with an increased risk of neurocognitive disorder. Therefore, early detection and treatment are essential.
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Affiliation(s)
- Mulualem Admasu Kelebie
- Department of Psychiatry, School of Medicine and Health Science, University of Gondar, College of Medicine and Health Sciences, Gondar, Ethiopia
| | - Techilo Tinsae
- Department of Psychiatry, School of Medicine and Health Science, University of Gondar, College of Medicine and Health Sciences, Gondar, Ethiopia
| | - Biruk Fanta Alemayehu
- Department of Psychiatry, School of Medicine and Health Science, University of Gondar, College of Medicine and Health Sciences, Gondar, Ethiopia
| | - Getasew Kibralew Walelign
- Department of Psychiatry, School of Medicine and Health Science, University of Gondar, College of Medicine and Health Sciences, Gondar, Ethiopia
| | - Girmaw Medfu Takelle
- Department of Psychiatry, School of Medicine and Health Sciences, University of Gondar College of Medicine and Health Sciences, Gondar, Amhara, Ethiopia
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Diener C, Gibbons SM. Metagenomic estimation of dietary intake from human stool. BIORXIV : THE PREPRINT SERVER FOR BIOLOGY 2024:2024.02.02.578701. [PMID: 38370672 PMCID: PMC10871216 DOI: 10.1101/2024.02.02.578701] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Grants] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 02/20/2024]
Abstract
Dietary intake is tightly coupled to gut microbiota composition, human metabolism, and to the incidence of virtually all major chronic diseases. Dietary and nutrient intake are usually quantified using dietary questionnaires, which tend to focus on broad food categories, suffer from self-reporting biases, and require strong compliance from study participants. Here, we present MEDI (Metagenomic Estimation of Dietary Intake): a method for quantifying dietary intake using food-derived DNA in stool metagenomes. We show that food items can be accurately detected in metagenomic shotgun sequencing data, even when present at low abundances (>10 reads). Furthermore, we show how dietary intake, in terms of DNA abundance from specific organisms, can be converted into a detailed metabolic representation of nutrient intake. MEDI could identify the onset of solid food consumption in infants and it accurately predicted food questionnaire responses in an adult population. Additionally, we were able to identify specific dietary features associated with metabolic syndrome in a large clinical cohort, providing a proof-of-concept for detailed quantification of individual-specific dietary patterns without the need for questionnaires.
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Affiliation(s)
- Christian Diener
- Diagnostic and Research Institute of Hygiene, Microbiology and Environmental Medicine, Medical University of Graz, Graz, Austria
- Institute for Systems Biology, Seattle, WA, USA
| | - Sean M. Gibbons
- Institute for Systems Biology, Seattle, WA, USA
- Department of Bioengineering, University of Washington, Seattle, WA, USA
- Department of Genome Sciences, University of Washington, Seattle, WA, USA
- eScience Institute, University of Washington, Seattle, WA, USA
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Rai S, Keservani RK, Kumar P, Nikam VK, Kachave RN, Kumar Y, Kesharwani RK. Importance of functional foods in the management of autism. NUTRACEUTICAL FRUITS AND FOODS FOR NEURODEGENERATIVE DISORDERS 2024:151-171. [DOI: 10.1016/b978-0-443-18951-7.00008-6] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 01/04/2025]
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Li C, Chen Z, He S, Chen Y, Liu J. Unveiling the influence of daily dietary patterns on brain cortical structure: insights from bidirectional Mendelian randomization. Food Funct 2023; 14:10418-10429. [PMID: 37960880 DOI: 10.1039/d3fo02879h] [Citation(s) in RCA: 6] [Impact Index Per Article: 3.0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/15/2023]
Abstract
Cognitive impairment is a significant concern in aging populations. This study utilized Mendelian randomization analysis to explore the impact of dietary habits and macro-nutrients on cortical structure. A bidirectional Mendelian randomization approach was employed, incorporating large-scale genetic data on dietary habits and brain cortical structure. The results did not reveal significant causal relationships between dietary factors and overall cortical structure and thickness. However, specific dietary factors showed associations with cortical structure in certain regions. For instance, fat intake affected six cortical regions, while milk, protein, fruits, and water were associated with changes in specific regions. Reverse analysis suggested that cortical thickness influenced the consumption of alcohol, carbohydrates, coffee, and fish. These findings contribute to understanding the potential mechanisms underlying the role of dietary factors in cognitive function changes and provide evidence supporting the existence of the gut-brain axis.
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Affiliation(s)
- Cong Li
- Department of Radiology, The Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, China.
| | - Zhe Chen
- Department of Thoracic Surgery, The Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, China
| | - Shaqi He
- Department of Radiology, The Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, China.
| | - Yanjing Chen
- Department of Radiology, The Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, China.
| | - Jun Liu
- Department of Radiology, The Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, China.
- Clinical Research Center for Medical Imaging in Hunan Province, Changsha, Hunan Province, 410011, People's Republic of China
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Chaudhary A, Prakash C, Sharma SK, Mor S, Ravindra K, Krishnan P. Health risk assessment of aerosol particles (PM 2.5 and PM 10) during winter crop at the agricultural site of Delhi, India. ENVIRONMENTAL MONITORING AND ASSESSMENT 2023; 195:1297. [PMID: 37828346 DOI: 10.1007/s10661-023-11826-1] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Received: 02/15/2023] [Accepted: 09/01/2023] [Indexed: 10/14/2023]
Abstract
For the last few decades, air pollution in developing country like India is increasing, and it is a matter of huge concern due to its associated human health impacts. In this region, the burgeoning population, escalating urbanization and industrialization, has been cited as the major reason for such a high air pollution. The present study was carried out for health risk assessment of aerosol particles (PM10 and PM2.5) and its associated heavy metals of an agriculture farm site at Indian Agricultural Research Institute (IARI) considered to be green urban area in Delhi, India. The concentrations of both PM10 and PM2.5 varied significantly from 136 to 177 µg/m3 and 56 to 162 µg/m3, respectively at the site. In the present case, the highest PM10 and PM2.5 levels were reported in January, followed by December. The levels of ambient PM10 and PM2.5 are influenced by wind prevailing meteorology. These levels of PM10 and PM2.5 are more than the permissible limits of WHO guidelines of 15 and 5 µg/m3, respectively, thereby leading to high aerosol loadings specifically in winters. The PM concentration of the atmosphere was found to be negatively correlated with temperature during the sampling period. The concentrations of surface ozone O3 and NOx in the present study were observed to be high in February and March, respectively. The increasing air pollution in the city of Delhi poses a great risk to the human health, as the particulate matter loaded with heavy metals can enter humans via different pathways, viz., ingestion, inhalation, and absorption through skin. The mean hazard index for metals (Zn, Pb, Cd, As, Cr, and Ni) was observed within the acceptable limit (HI < 1), thereby indicating negligible non-carcinogenic effects to residing population. The carcinogenic risk assessment was conducted for Cd, Pb, and As only, as the concentrations for other metals were found to be quite low. The carcinogenic risk values were also within the limits of USEPA standards, indicating no carcinogenic risks to the health of children and adults residing near the site. This information about the PM pollution at the agricultural site and health risk assessment will serve as a baseline data in assessment of human health impacts due to air pollution at the local scale and can be used for development of mitigation strategies for tackling air pollution.
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Affiliation(s)
- Anita Chaudhary
- Division of Environment Sciences, ICAR-IARI, New Delhi, 110 012, India.
| | - Chandra Prakash
- Division of Environment Sciences, ICAR-IARI, New Delhi, 110 012, India
| | - Sudhir Kumar Sharma
- CSIR-National Physical Laboratory, Dr. K.S. Krishnan Road, New Delhi, 110012, India
| | - Suman Mor
- Department of Environment Studies, Panjab University, Chandigarh, 160014, India
| | - Khaiwal Ravindra
- Department of Community Medicine and School of Public Health, PGIMER, Chandigarh, 160015, India
| | - Prameela Krishnan
- Division of Agricultural Physics, ICAR-IARI, New Delhi, 110 012, India
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Fituri S, Shi Z. Association between Dietary Patterns and Cognitive Function among Qatari Adults: A Cross-Sectional Analysis of the Qatar Biobank Study. Nutrients 2023; 15:4053. [PMID: 37764836 PMCID: PMC10537779 DOI: 10.3390/nu15184053] [Citation(s) in RCA: 2] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/27/2023] [Revised: 09/11/2023] [Accepted: 09/16/2023] [Indexed: 09/29/2023] Open
Abstract
This study aimed to assess the association between dietary patterns and cognitive function among Qatari adults. In a cross-sectional analysis, data on 1000 Qatari adults attending the Qatar Biobank Study (QBB) aged ≥18 years were obtained. Using factor analysis, dietary patterns were constructed based on habitual dietary intake assessed by food frequency questionnaires (FFQs). The mean reaction time (MRT) derived from self-administered touch screen tests was used as an indicator of cognitive function. The association between dietary patterns and MRT was investigated using linear regression. The mean age of the participants was 35.8 (SD 10.3) years, and the mean MRT was 715.3 (SD 204.1) milliseconds. Three dietary patterns were identified. The "traditional" dietary pattern, characterized by high intakes of white rice, mixed dishes and soups/starters possibly high in saturated fat and sodium, was positively associated with MRT. In the multivariable model, comparing the highest to lowest quartiles of the traditional pattern, the regression coefficient for MRT was 50.0 (95% CI 16.9, 83.1; p for trend 0.001). There was an effect modification of diabetes and age on the association between the "modern" dietary pattern and MRT. The "convenient" dietary pattern was not associated with cognition. In conclusion, the traditional rice-based dietary pattern may be associated with poor cognitive function.
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Affiliation(s)
| | - Zumin Shi
- Human Nutrition Department, College of Health Sciences, QU Health, Qatar University, Doha P.O. Box 2713, Qatar;
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Elizaldi SR, Verma A, Ma ZM, Ott S, Rajasundaram D, Cottrell ML, Kashuba ADM, Ambrose Z, Lifson JD, Morrison JH, Iyer SS. CD4 T cell Responses in the CNS during SIV infection. BIORXIV : THE PREPRINT SERVER FOR BIOLOGY 2023:2023.08.24.554055. [PMID: 37662237 PMCID: PMC10473718 DOI: 10.1101/2023.08.24.554055] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Grants] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 09/05/2023]
Abstract
Virologic suppression with antiretroviral therapy (ART) has significantly improved health outcomes for people living with HIV, yet challenges related to chronic inflammation in the central nervous system (CNS) - known as Neuro-HIV- persist. As primary targets for HIV-1 with the ability to survey and populate the CNS and interact with myeloid cells to co-ordinate neuroinflammation, CD4 T cells are pivotal in Neuro-HIV. Despite their importance, our understanding of CD4 T cell distribution in virus-targeted CNS tissues, their response to infection, and potential recovery following initiation of ART remain limited. To address these gaps, we studied ten SIVmac251-infected rhesus macaques using an ART regimen simulating suboptimal adherence. We evaluated four macaques during the acute phase pre-ART and six during the chronic phase. Our data revealed that HIV target CCR5+ CD4 T cells inhabit both the brain parenchyma and adjacent CNS tissues, encompassing choroid plexus stroma, dura mater, and the skull bone marrow. Aligning with the known susceptibility of CCR5+ CD4 T cells to viral infection and their presence within the CNS, high levels of viral RNA were detected in the brain parenchyma and its border tissues during acute SIV infection. Single-cell RNA sequencing of CD45+ cells from the brain revealed colocalization of viral transcripts within CD4 clusters and significant activation of antiviral molecules and specific effector programs within T cells, indicating CNS CD4 T cell engagement during infection. Despite viral suppression with ART, acute infection led to significant depletion of CNS CD4 T cells, persisting into the chronic phase. These findings underscore the functional involvement of CD4 T cells within the CNS during SIV infection, enhancing our understanding of their role in establishing CNS viral presence. Our results offer insights for potential T cell-focused interventions while also underscoring the challenges in eradicating HIV from the CNS, even with effective ART.
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Affiliation(s)
| | - Anil Verma
- Department of Pathology, School of Medicine, University of Pittsburgh, PA, USA
| | - Zhong-Min Ma
- California National Primate Research Center, UC Davis, CA, USA
| | - Sean Ott
- California National Primate Research Center, UC Davis, CA, USA
| | | | | | - Angela D M Kashuba
- Eshelman School of Pharmacy, University of North Carolina, Chapel Hill, NC, USA
| | - Zandrea Ambrose
- Department of Microbiology and Molecular Genetics, School of Medicine, University of Pittsburgh, PA, USA
| | - Jeffrey D Lifson
- AIDS and Cancer Virus Program, Frederick National Laboratory, Frederick, MD, USA
| | - John H Morrison
- California National Primate Research Center, UC Davis, CA, USA
- Department of Neurology, School of Medicine, UC Davis, CA,USA
| | - Smita S Iyer
- Department of Pathology, School of Medicine, University of Pittsburgh, PA, USA
- California National Primate Research Center, UC Davis, CA, USA
- Department of Pathology, Microbiology, and Immunology, School of Veterinary Medicine, UC Davis, CA,USA
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11
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Hashemi R, Vahabi Z, Rasekhi H, Shiraseb F, Amini M. Dietary patterns and the risk of Alzheimer's disease in an elderly Iranian population: a case-control study. JOURNAL OF HEALTH, POPULATION, AND NUTRITION 2023; 42:56. [PMID: 37322540 DOI: 10.1186/s41043-023-00398-y] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Subscribe] [Scholar Register] [Received: 03/03/2023] [Accepted: 06/09/2023] [Indexed: 06/17/2023]
Abstract
BACKGROUND An increasing number of studies in Western countries have shown that healthy eating patterns have a protective effect against cognitive decline and dementia, however, information about this relationship among non-western populations with different cultural environments is scarce. The present study investigated the association between dietary patterns (DPs) and cognitive function in the Iranian elderly. METHODS In this case-control study, the data of 290 elderly people in two groups of case and control (Mean age in case: 74.2 ± 8.6, in control: 67.3 ± 7.3 year) were analyzed. Two DPs of healthy and unhealthy were extracted from a 142-item dish-based food frequency questionnaire, and patterns driven by principal components analysis (PCA) of 25 food groups. Multivariate binary logistic regression calculated the odds ratio (OR) of cognitive impairment with adjustment for potential confounding factors. RESULTS A healthy DP, characterized by high consumption of fruits and vegetables, legumes, and nuts, was related to a decrease in the odds of Alzheimer's disease in Iranian elderly people. Also, moderate adherence to an unhealthy food pattern was associated with an increase in the probability of the disease; however, the association was not statistically significant. CONCLUSION In this elderly population, a healthy eating pattern was associated with reducing the risk of Alzheimer's disease. Further prospective studies are recommended.
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Affiliation(s)
- Rezvan Hashemi
- Department of Geriatric Medicine, Ziaeian Hospital, Tehran University of Medical Sciences, Tehran, Iran
| | - Zahra Vahabi
- Geriatric Department, Tehran University of Medical Sciences, Tehran, Iran
- Neurology Division, CNS Department, Western University, London, ON, Canada
| | - Hamid Rasekhi
- Department of Nutrition Research, National Nutrition and Food Technology Research Institute and Faculty of Nutrition Sciences and Food Technology, Shahid Beheshti University of Medical Sciences, Tehran, Iran
| | - Farideh Shiraseb
- Department of Community Nutrition, School of Nutritional Sciences and Dietetics, Tehran University of Medical Sciences, Tehran, Iran
| | - Maryam Amini
- Department of Nutrition Research, National Nutrition and Food Technology Research Institute and Faculty of Nutrition Sciences and Food Technology, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
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12
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Flores AC, Jensen GL, Mitchell DC, Na M, Wood GC, Still CD, Gao X. Prospective Study of Diet Quality and the Risk of Dementia in the Oldest Old. Nutrients 2023; 15:nu15051282. [PMID: 36904280 PMCID: PMC10005581 DOI: 10.3390/nu15051282] [Citation(s) in RCA: 3] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/04/2023] [Revised: 02/24/2023] [Accepted: 02/28/2023] [Indexed: 03/08/2023] Open
Abstract
This study examined the associations between overall diet quality and the risk of dementia in a rural cohort among the oldest old. Included in this prospective cohort study were 2232 participants aged ≥ 80 years and dementia-free at the baseline according to the Geisinger Rural Aging Study (GRAS), a longitudinal cohort in rural Pennsylvania. In 2009, diet quality was assessed by a validated dietary screening tool (DST). Incident cases of dementia during 2009-2021 were identified using diagnosis codes. This approach was validated by a review of electronic health records. Associations between diet quality scores and the incidence of dementia were estimated using the Cox proportional hazards models, adjusted for potential confounders. Across a mean of 6.90 years of follow-up, we identified 408 incident cases of all-cause dementia. Having a higher diet quality was not significantly associated with a lower risk for incidents of all-cause dementia (adjusted HR for the highest compared with the lowest tertile: 1.01, 95% CI: 0.79, 1.29, P-trend = 0.95). Similarly, we did not observe a significant association between diet quality and altered risks of Alzheimer's disease and other forms of dementia. Overall, having a higher diet quality was not significantly associated with a lower risk of dementia among the oldest old during the full follow-up.
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Affiliation(s)
- Ashley C. Flores
- Department of Nutritional Sciences, The Pennsylvania State University, State College, PA 16801, USA
| | - Gordon L. Jensen
- Larner College of Medicine, University of Vermont, Burlington, VT 05405, USA
| | - Diane C. Mitchell
- Department of Nutritional Sciences, The Pennsylvania State University, State College, PA 16801, USA
| | - Muzi Na
- Department of Nutritional Sciences, The Pennsylvania State University, State College, PA 16801, USA
| | - G. Craig Wood
- Obesity Institute, Geisinger Health System, Danville, PA 17822, USA
| | | | - Xiang Gao
- Department of Nutritional Sciences, The Pennsylvania State University, State College, PA 16801, USA
- School of Public Health, Institute of Nutrition, Fudan University, Shanghai 200437, China
- Correspondence:
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13
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Maggi S, Ticinesi A, Limongi F, Noale M, Ecarnot F. The role of nutrition and the Mediterranean diet on the trajectories of cognitive decline. Exp Gerontol 2023; 173:112110. [PMID: 36720373 DOI: 10.1016/j.exger.2023.112110] [Citation(s) in RCA: 16] [Impact Index Per Article: 8.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/05/2022] [Revised: 01/16/2023] [Accepted: 01/27/2023] [Indexed: 02/02/2023]
Abstract
The worldwide burden of dementia is immense, and set to increase to unprecedented levels in the coming decades, due to population aging. In the absence of disease-modifying treatment, there is therefore a strong rationale to support the assumption that acting on modifiable risk factors, especially in midlife, is a good strategy for reducing the burden of dementia. Among these risk factors, nutrition is key, as it is fundamental to healthy aging, and has interrelated benefits on a number of organ systems, metabolic processes and health states that can all contribute to modifying the risk of dementia. In this paper, we review the methodological challenges of comparing studies of dietary interventions. We then discuss the effect of genetics and the environment on brain health, and review in particular the literature data on the effect of nutrition on cognition. We summarize the body of data reporting the largely beneficial effects of the Mediterranean diet on brain health, and the possible mechanisms that mediate these effects. Finally, we discuss future perspectives for further research in the field, notably the "gut-brain axis", thought to be a key mediator of the effect of nutrition on brain health.
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Affiliation(s)
- Stefania Maggi
- National Research Council, Neuroscience Institute, Aging Branch, Padova, Italy
| | - Andrea Ticinesi
- Department of Medicine and Surgery, University of Parma, Geriatric-Rehabilitation Department, Parma University-Hospital, Parma, Italy
| | - Federica Limongi
- National Research Council, Neuroscience Institute, Aging Branch, Padova, Italy
| | - Marianna Noale
- National Research Council, Neuroscience Institute, Aging Branch, Padova, Italy
| | - Fiona Ecarnot
- University Hospital, Research Unit EA3920, University of Franche-Comté, 25000 Besançon, France.
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14
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Khan S, Hassan MI, Shahid M, Islam A. Nature's Toolbox Against Tau Aggregation: An Updated Review of Current Research. Ageing Res Rev 2023; 87:101924. [PMID: 37004844 DOI: 10.1016/j.arr.2023.101924] [Citation(s) in RCA: 2] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/16/2023] [Revised: 03/21/2023] [Accepted: 03/30/2023] [Indexed: 04/03/2023]
Abstract
Tau aggregation is a hallmark of several neurodegenerative disorders, such as Alzheimer's disease (AD), frontotemporal dementia, and progressive supranuclear palsy. Hyperphosphorylated tau is believed to contribute to the degeneration of neurons and the development of these complex diseases. Therefore, one potential treatment for these illnesses is to prevent or counteract tau aggregation. In recent years, interest has been increasing in developing nature-derived tau aggregation inhibitors as a potential treatment for neurodegenerative disorders. Researchers have become increasingly interested in natural compounds with multifunctional features, such as flavonoids, alkaloids, resveratrol, and curcumin, since these molecules can interact simultaneously with the various targets of AD. Recent studies have demonstrated that several natural compounds can inhibit tau aggregation and promote the disassembly of pre-formed tau aggregates. Nature-derived tau aggregation inhibitors hold promise as a potential treatment for neurodegenerative disorders. However, it is important to note that more research is needed to fully understand the mechanisms by which these compounds exert their effects and their safety and efficacy in preclinical and clinical studies. Nature-derived inhibitors of tau aggregation are a promising new direction in the research of neurodegenerative complexities. This review focuses on the natural products that have proven to be a rich supply for inhibitors in tau aggregation and their uses in neurodegenerative complexities, including AD.
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15
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Comparison of Oleocanthal-Low EVOO and Oleocanthal against Amyloid-β and Related Pathology in a Mouse Model of Alzheimer's Disease. Molecules 2023; 28:molecules28031249. [PMID: 36770920 PMCID: PMC9921117 DOI: 10.3390/molecules28031249] [Citation(s) in RCA: 6] [Impact Index Per Article: 3.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/15/2022] [Revised: 01/06/2023] [Accepted: 01/25/2023] [Indexed: 01/31/2023] Open
Abstract
Alzheimer's disease (AD) is characterized by several pathological hallmarks, including the deposition of amyloid-β (Aβ) plaques, neurofibrillary tangles, blood-brain barrier (BBB) dysfunction, and neuroinflammation. Growing evidence support the neuroprotective effects of extra-virgin olive oil (EVOO) and oleocanthal (OC). In this work, we aimed to evaluate and compare the beneficial effects of equivalent doses of OC-low EVOO (0.5 mg total phenolic content/kg) and OC (0.5 mg OC/kg) on Aβ and related pathology and to assess their effect on neuroinflammation in a 5xFAD mouse model with advanced pathology. Homozygous 5xFAD mice were fed with refined olive oil (ROO), OC-low EVOO, or OC for 3 months starting at the age of 3 months. Our findings demonstrated that a low dose of 0.5 mg/kg EVOO-phenols and OC reduced brain Aβ levels and neuroinflammation by suppressing the nuclear factor-κB (NF-κB) pathway and reducing the activation of NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3) inflammasomes. On the other hand, only OC suppressed the receptor for advanced glycation endproducts/high-mobility group box 1 (RAGE/HMGB1) pathway. In conclusion, our results indicated that while OC-low EVOO demonstrated a beneficial effect against Aβ-related pathology in 5xFAD mice, EVOO rich with OC could provide a higher anti-inflammatory effect by targeting multiple mechanisms. Collectively, diet supplementation with EVOO or OC could prevent, halt progression, and treat AD.
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16
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Townsend RF, Logan D, O’Neill RF, Prinelli F, Woodside JV, McEvoy CT. Whole Dietary Patterns, Cognitive Decline and Cognitive Disorders: A Systematic Review of Prospective and Intervention Studies. Nutrients 2023; 15:nu15020333. [PMID: 36678204 PMCID: PMC9865080 DOI: 10.3390/nu15020333] [Citation(s) in RCA: 7] [Impact Index Per Article: 3.5] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/07/2022] [Revised: 12/17/2022] [Accepted: 12/21/2022] [Indexed: 01/12/2023] Open
Abstract
Dementia prevalence is a global public health concern. Adherence towards a healthy dietary pattern (DP) may reduce the risk of cognitive decline and dementia. This narrative systematic review aimed to synthesise prospective and intervention study data to evaluate the impact of a-posteriori and a-priori derived DPs on cognitive ageing, from cognitive decline to incident dementia. Ninety-three studies were included: 83 prospective studies and 10 randomised controlled trials (RCT). Most prospective studies (77%) examined a-priori DPs, with the Mediterranean diet examined most frequently. A total of 52% of prospective and 50% of RCTs reported a protective relationship between 'healthy' DPs and global cognitive decline. Overall, 59% of prospective studies reported positive associations between healthy DPs and risk of cognitive disorder. Incident cognitive disorder was examined by only one intervention study (subgroup analysis) which reported a beneficial effect of a low-fat diet on risk of probable dementia in women. Unhealthy DPs were examined less frequently (n = 17; 21%), with 41% of these studies reporting associations between adherence and poorer cognitive outcomes. Overall, there were mixed results for healthy and unhealthy DPs on cognition, likely due to between-study heterogeneity. Standardisation of diet exposure and cognitive outcome measurement would help to reduce this. Future research would benefit from investigating effects of culturally appropriate DPs on individual cognitive domains and incident cognitive disorders in diverse and high-risk populations.
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Affiliation(s)
| | - Danielle Logan
- Centre for Public Health, Queen’s University Belfast, Belfast BT12 6BA, UK
| | - Roisin F. O’Neill
- Centre for Public Health, Queen’s University Belfast, Belfast BT12 6BA, UK
| | - Federica Prinelli
- Epidemiology Unit, Institute of Biomedical Technologies, National Research Council, 93 20054 Milan, Italy
| | - Jayne V. Woodside
- Centre for Public Health, Queen’s University Belfast, Belfast BT12 6BA, UK
- Institute for Global Food Security, Queen’s University Belfast, Belfast BT9 5DL, UK
| | - Claire T. McEvoy
- Centre for Public Health, Queen’s University Belfast, Belfast BT12 6BA, UK
- Institute for Global Food Security, Queen’s University Belfast, Belfast BT9 5DL, UK
- Correspondence:
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Shang X, Roccati E, Zhu Z, Kiburg K, Wang W, Huang Y, Zhang X, Zhang X, Liu J, Tang S, Hu Y, Ge Z, Yu H, He M. Leading mediators of sex differences in the incidence of dementia in community-dwelling adults in the UK Biobank: a retrospective cohort study. Alzheimers Res Ther 2023; 15:7. [PMID: 36617573 PMCID: PMC9827665 DOI: 10.1186/s13195-022-01140-2] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/14/2022] [Accepted: 12/08/2022] [Indexed: 01/10/2023]
Abstract
BACKGROUND Little is known regarding whether sex assigned at birth modifies the association between several predictive factors for dementia and the risk of dementia itself. METHODS Our retrospective cohort study included 214,670 men and 214,670 women matched by age at baseline from the UK Biobank. Baseline data were collected between 2006 and 2010, and incident dementia was ascertained using hospital inpatient or death records until January 2021. Mediation analysis was tested for 133 individual factors. RESULTS Over 5,117,381 person-years of follow-up, 5928 cases of incident all-cause dementia (452 cases of young-onset dementia, 5476 cases of late-onset dementia) were documented. Hazard ratios (95% CI) for all-cause, young-onset, and late-onset dementias associated with the male sex (female as reference) were 1.23 (1.17-1.29), 1.42 (1.18-1.71), and 1.21 (1.15-1.28), respectively. Out of 133 individual factors, the strongest mediators for the association between sex and incident dementia were multimorbidity risk score (percentage explained (95% CI): 62.1% (45.2-76.6%)), apolipoprotein A in the blood (25.5% (15.2-39.4%)), creatinine in urine (24.9% (16.1-36.5%)), low-density lipoprotein cholesterol in the blood (23.2% (16.2-32.1%)), and blood lymphocyte percentage (21.1% (14.5-29.5%)). Health-related conditions (percentage (95% CI) explained: 74.4% (51.3-88.9%)) and biomarkers (83.0% (37.5-97.5%)), but not lifestyle factors combined (30.1% (20.7-41.6%)), fully mediated sex differences in incident dementia. Health-related conditions combined were a stronger mediator for late-onset (75.4% (48.6-90.8%)) than for young-onset dementia (52.3% (25.8-77.6%)), whilst lifestyle factors combined were a stronger mediator for young-onset (42.3% (19.4-69.0%)) than for late-onset dementia (26.7% (17.1-39.2%)). CONCLUSIONS Our analysis matched by age has demonstrated that men had a higher risk of all-cause, young-onset, and late-onset dementias than women. This association was fully mediated by health-related conditions or blood/urinary biomarkers and largely mediated by lifestyle factors. Our findings are important for understanding potential mechanisms of sex in dementia risk.
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Affiliation(s)
- Xianwen Shang
- Guangdong Eye Institute, Department of Ophthalmology, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, 510080, China.
- Guangdong Cardiovascular Institute, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, 510080, China.
- Centre for Eye Research Australia, Melbourne, VIC, 3002, Australia.
- Department of Medicine (Royal Melbourne Hospital), University of Melbourne, Melbourne, VIC, 3050, Australia.
| | - Eddy Roccati
- Department of Medicine (Royal Melbourne Hospital), University of Melbourne, Melbourne, VIC, 3050, Australia
- Wicking Dementia Research and Education Centre, University of Tasmania, Hobart, TAS, 7001, Australia
| | - Zhuoting Zhu
- Guangdong Eye Institute, Department of Ophthalmology, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, 510080, China
- Guangdong Cardiovascular Institute, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, 510080, China
- Centre for Eye Research Australia, Melbourne, VIC, 3002, Australia
| | - Katerina Kiburg
- Centre for Eye Research Australia, Melbourne, VIC, 3002, Australia
| | - Wei Wang
- State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou, 510060, China
| | - Yu Huang
- Guangdong Eye Institute, Department of Ophthalmology, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, 510080, China
- Guangdong Cardiovascular Institute, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, 510080, China
| | - Xueli Zhang
- Guangdong Eye Institute, Department of Ophthalmology, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, 510080, China
| | - Xiayin Zhang
- Guangdong Eye Institute, Department of Ophthalmology, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, 510080, China
- Guangdong Cardiovascular Institute, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, 510080, China
| | - Jiahao Liu
- Centre for Eye Research Australia, Melbourne, VIC, 3002, Australia
| | - Shulin Tang
- Guangdong Eye Institute, Department of Ophthalmology, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, 510080, China
| | - Yijun Hu
- Guangdong Eye Institute, Department of Ophthalmology, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, 510080, China
| | - Zongyuan Ge
- Monash e-Research Center, Faculty of Engineering, Airdoc Research, Nvidia AI Technology Research Center, Monash University, Melbourne, VIC, 3800, Australia
| | - Honghua Yu
- Guangdong Eye Institute, Department of Ophthalmology, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, 510080, China.
| | - Mingguang He
- Guangdong Eye Institute, Department of Ophthalmology, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, 510080, China.
- Centre for Eye Research Australia, Melbourne, VIC, 3002, Australia.
- State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou, 510060, China.
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Kalia V, Kulick ER, Vardarajan B, Gu Y, Manly JJ, Elkind MS, Kaufman JD, Jones DP, Baccarelli AA, Mayeux R, Kioumourtzoglou MA, Miller GW. Linking Air Pollution Exposure to Blood-Based Metabolic Features in a Community-Based Aging Cohort with and without Dementia. J Alzheimers Dis 2023; 96:1025-1040. [PMID: 37927256 PMCID: PMC10741333 DOI: 10.3233/jad-230122] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Accepted: 09/11/2023] [Indexed: 11/07/2023]
Abstract
BACKGROUND Long-term exposure to air pollution has been associated with changes in levels of metabolites measured in the peripheral blood. However, most research has been conducted in ethnically homogenous, young or middle-aged populations. OBJECTIVE To study the relationship between the plasma metabolome and long-term exposure to three air pollutants: particulate matter (PM) less than 2.5μm in aerodynamic diameter (PM2.5), PM less than 10μm in aerodynamic diameter (PM10), and nitrogen dioxide (NO2) in an ethnically diverse, older population. METHODS Plasma metabolomic profiles of 107 participants of the Washington Heights and Inwood Community Aging Project in New York City, collected from 1995-2015, including non-Hispanic white, Caribbean Hispanic, and non-Hispanic Black older adults were used. We estimated the association between each metabolic feature and predicted annual mean exposure to the air pollutants using three approaches: 1) A metabolome wide association study framework; 2) Feature selection using elastic net regression; and 3) A multivariate approach using partial-least squares discriminant analysis. RESULTS 79 features associated with exposure to PM2.5 but none associated with PM10 or NO2. PM2.5 exposure was associated with altered amino acid metabolism, energy production, and oxidative stress response, pathways also associated with Alzheimer's disease. Three metabolites were associated with PM2.5 exposure through all three approaches: cysteinylglycine disulfide, a diglyceride, and a dicarboxylic acid. The relationship between several features and PM2.5 exposure was modified by diet and metabolic diseases. CONCLUSIONS These relationships uncover the mechanisms through which PM2.5 exposure can lead to altered metabolic outcomes in an older population.
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Affiliation(s)
- Vrinda Kalia
- Department of Environmental Health Sciences, Mailman School of Public Health, Columbia University, New York, NY, USA
| | - Erin R. Kulick
- Department of Epidemiology and Biostatistics, Temple University College of Public Health, Philadelphia, PA, USA
| | - Badri Vardarajan
- Taub Institute for Research on Alzheimer’s Disease and the Aging Brain, Vagelos College of Physicians and Surgeons, Columbia University, New York, NY, USA
- The Gertrude H. Sergievsky Center, Vagelos College of Physicians and Surgeons, Columbia University, New York, NY, USA
- Department of Neurology, Vagelos College of Physicians and Surgeons, Columbia University and the New York Presbyterian Hospital, New York, NY, USA
| | - Yian Gu
- Taub Institute for Research on Alzheimer’s Disease and the Aging Brain, Vagelos College of Physicians and Surgeons, Columbia University, New York, NY, USA
- The Gertrude H. Sergievsky Center, Vagelos College of Physicians and Surgeons, Columbia University, New York, NY, USA
- Department of Neurology, Vagelos College of Physicians and Surgeons, Columbia University and the New York Presbyterian Hospital, New York, NY, USA
- Department of Epidemiology, Mailman School of Public Health, Columbia University, New York, NY, USA
| | - Jennifer J. Manly
- Taub Institute for Research on Alzheimer’s Disease and the Aging Brain, Vagelos College of Physicians and Surgeons, Columbia University, New York, NY, USA
- Department of Neurology, Vagelos College of Physicians and Surgeons, Columbia University and the New York Presbyterian Hospital, New York, NY, USA
| | - Mitchell S.V. Elkind
- The Gertrude H. Sergievsky Center, Vagelos College of Physicians and Surgeons, Columbia University, New York, NY, USA
- Department of Neurology, Vagelos College of Physicians and Surgeons, Columbia University and the New York Presbyterian Hospital, New York, NY, USA
- Department of Epidemiology, Mailman School of Public Health, Columbia University, New York, NY, USA
| | - Joel D. Kaufman
- Departments of Environmental and Occupational Health Sciences, Medicine, and Epidemiology, University of Washington, Seattle, WA, USA
| | - Dean P. Jones
- Department of Medicine, Clinical Biomarkers Laboratory, Emory University, Atlanta, GA, USA
| | - Andrea A. Baccarelli
- Department of Environmental Health Sciences, Mailman School of Public Health, Columbia University, New York, NY, USA
| | - Richard Mayeux
- Taub Institute for Research on Alzheimer’s Disease and the Aging Brain, Vagelos College of Physicians and Surgeons, Columbia University, New York, NY, USA
- The Gertrude H. Sergievsky Center, Vagelos College of Physicians and Surgeons, Columbia University, New York, NY, USA
- Department of Neurology, Vagelos College of Physicians and Surgeons, Columbia University and the New York Presbyterian Hospital, New York, NY, USA
- Department of Epidemiology, Mailman School of Public Health, Columbia University, New York, NY, USA
- Department of Psychiatry, Vagelos College of Physicians and Surgeons, Columbia University, New York, NY, USA
| | | | - Gary W. Miller
- Department of Environmental Health Sciences, Mailman School of Public Health, Columbia University, New York, NY, USA
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Gou R, Qin J, Pang W, Cai J, Luo T, He K, Xiao S, Tang X, Zhang Z, Li Y. Correlation between dietary patterns and cognitive function in older Chinese adults: A representative cross-sectional study. Front Nutr 2023; 10:1093456. [PMID: 37081915 PMCID: PMC10110985 DOI: 10.3389/fnut.2023.1093456] [Citation(s) in RCA: 3] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/09/2022] [Accepted: 03/13/2023] [Indexed: 04/22/2023] Open
Abstract
Objective The objective of this study was to investigate the relationship between dietary patterns and cognitive function in older adults (≥60 years old). Methods Food intake was quantitatively assessed by the Food Frequency Questionnaire (FFQ), and cognitive function was assessed by the Chinese version of the Simple Mental State Examination Scale (MMSE). Four major dietary patterns were identified by the factor analysis (FA) method. The relationship between dietary patterns and cognitive function was evaluated by logistic regression. Results A total of 884 participants were included in the study. Four dietary patterns (vegetable and mushroom, oil and salt, seafood and alcohol, and oil tea dietary patterns) were extracted. In the total population, Model III results showed that the fourth quartile of dietary pattern factor scores for the vegetable and mushroom pattern was 0.399 and 7.056. The vegetable and mushroom dietary pattern may be a protective factor for cognitive function, with p-value = 0.033, OR (95% CI): 0.578 (0.348, 0.951) in Model III (adjusted for covariates: sex, ethnic, marital, agricultural activities, smoking, drinking, hypertension, diabetes, dyslipidemia, BMI, and dietary fiber). In the ethnic stratification analysis, the scores of dietary pattern factors of the vegetable and mushroom among the Yao participants were 0.333 and 5.064. The Vegetable and mushroom diet pattern may be a protective factor for cognitive function, p-value = 0.012, OR (95% CI): 0.415 (0.206, 0.815). Conclusion The fourth quartile of the vegetable and mushroom dietary pattern scores showed dose-dependent and a strong correlation with cognitive function. Currently, increasing vegetable and mushroom intake may be one of the effective ways to prevent and mitigate cognitive decline. It is recommended to increase the dietary intake of vegetables and mushroom foods.
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Affiliation(s)
- Ruoyu Gou
- Department of Environmental Health and Occupational Medicine, School of Public Health, Guilin Medical University, Guilin, Guangxi, China
- The Guangxi Key Laboratory of Environmental Exposomics and Entire Lifecycle Heath, Guilin, Guangxi, China
| | - Jian Qin
- Department of Environmental and Occupational Health, School of Public Health, Guangxi Medical University, Nanning, Guangxi, China
| | - Weiyi Pang
- Department of Environmental Health and Occupational Medicine, School of Public Health, Guilin Medical University, Guilin, Guangxi, China
- The Guangxi Key Laboratory of Environmental Exposomics and Entire Lifecycle Heath, Guilin, Guangxi, China
| | - Jiansheng Cai
- Department of Environmental and Occupational Health, School of Public Health, Guangxi Medical University, Nanning, Guangxi, China
| | - Tingyu Luo
- Department of Environmental Health and Occupational Medicine, School of Public Health, Guilin Medical University, Guilin, Guangxi, China
- The Guangxi Key Laboratory of Environmental Exposomics and Entire Lifecycle Heath, Guilin, Guangxi, China
| | - Kailian He
- Department of Environmental Health and Occupational Medicine, School of Public Health, Guilin Medical University, Guilin, Guangxi, China
- The Guangxi Key Laboratory of Environmental Exposomics and Entire Lifecycle Heath, Guilin, Guangxi, China
| | - Song Xiao
- Department of Environmental Health and Occupational Medicine, School of Public Health, Guilin Medical University, Guilin, Guangxi, China
- The Guangxi Key Laboratory of Environmental Exposomics and Entire Lifecycle Heath, Guilin, Guangxi, China
| | - Xu Tang
- Department of Environmental and Occupational Health, School of Public Health, Guangxi Medical University, Nanning, Guangxi, China
| | - Zhiyong Zhang
- Department of Environmental Health and Occupational Medicine, School of Public Health, Guilin Medical University, Guilin, Guangxi, China
- The Guangxi Key Laboratory of Environmental Exposomics and Entire Lifecycle Heath, Guilin, Guangxi, China
- *Correspondence: Zhiyong Zhang
| | - You Li
- Department of Environmental Health and Occupational Medicine, School of Public Health, Guilin Medical University, Guilin, Guangxi, China
- The Guangxi Key Laboratory of Environmental Exposomics and Entire Lifecycle Heath, Guilin, Guangxi, China
- You Li
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Bramen JE, Siddarth P, Popa ES, Kress GT, Rapozo MK, Hodes JF, Ganapathi AS, Slyapich CB, Glatt RM, Pierce K, Porter VR, Wong C, Kim M, Dye RV, Panos S, Bookheimer T, Togashi T, Loong S, Raji CA, Bookheimer SY, Roach JC, Merrill DA. Impact of Eating a Carbohydrate-Restricted Diet on Cortical Atrophy in a Cross-Section of Amyloid Positive Patients with Alzheimer's Disease: A Small Sample Study. J Alzheimers Dis 2023; 96:329-342. [PMID: 37742646 PMCID: PMC10657694 DOI: 10.3233/jad-230458] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Accepted: 08/22/2023] [Indexed: 09/26/2023]
Abstract
BACKGROUND A carbohydrate-restricted diet aimed at lowering insulin levels has the potential to slow Alzheimer's disease (AD). Restricting carbohydrate consumption reduces insulin resistance, which could improve glucose uptake and neural health. A hallmark feature of AD is widespread cortical thinning; however, no study has demonstrated that lower net carbohydrate (nCHO) intake is linked to attenuated cortical atrophy in patients with AD and confirmed amyloidosis. OBJECTIVE We tested the hypothesis that individuals with AD and confirmed amyloid burden eating a carbohydrate-restricted diet have thicker cortex than those eating a moderate-to-high carbohydrate diet. METHODS A total of 31 patients (mean age 71.4±7.0 years) with AD and confirmed amyloid burden were divided into two groups based on a 130 g/day nCHO cutoff. Cortical thickness was estimated from T1-weighted MRI using FreeSurfer. Cortical surface analyses were corrected for multiple comparisons using cluster-wise probability. We assessed group differences using a two-tailed two-independent sample t-test. Linear regression analyses using nCHO as a continuous variable, accounting for confounders, were also conducted. RESULTS The lower nCHO group had significantly thicker cortex within somatomotor and visual networks. Linear regression analysis revealed that lower nCHO intake levels had a significant association with cortical thickness within the frontoparietal, cingulo-opercular, and visual networks. CONCLUSIONS Restricting carbohydrates may be associated with reduced atrophy in patients with AD. Lowering nCHO to under 130 g/day would allow patients to follow the well-validated MIND diet while benefiting from lower insulin levels.
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Affiliation(s)
- Jennifer E. Bramen
- Pacific Brain Health Center, Pacific Neuroscience Institute and Foundation, Santa Monica, CA, USA
- Saint John’s Cancer Institute at Providence Saint John’s Health Center, Santa Monica, CA, USA
- Providence Saint John’s Health Center, Santa Monica, CA, USA
| | - Prabha Siddarth
- Pacific Brain Health Center, Pacific Neuroscience Institute and Foundation, Santa Monica, CA, USA
- David Geffen School of Medicine at University of California Los Angeles, Los Angeles, CA, USA
| | - Emily S. Popa
- Pacific Brain Health Center, Pacific Neuroscience Institute and Foundation, Santa Monica, CA, USA
| | - Gavin T. Kress
- Pacific Brain Health Center, Pacific Neuroscience Institute and Foundation, Santa Monica, CA, USA
- Keck School of Medicine, University of Southern California, Los Angeles, CA, USA
| | - Molly K. Rapozo
- Pacific Brain Health Center, Pacific Neuroscience Institute and Foundation, Santa Monica, CA, USA
| | - John F. Hodes
- Pacific Brain Health Center, Pacific Neuroscience Institute and Foundation, Santa Monica, CA, USA
- Drexel University College of Medicine, Philadelphia, PA, USA
| | - Aarthi S. Ganapathi
- Pacific Brain Health Center, Pacific Neuroscience Institute and Foundation, Santa Monica, CA, USA
| | - Colby B. Slyapich
- Pacific Brain Health Center, Pacific Neuroscience Institute and Foundation, Santa Monica, CA, USA
| | - Ryan M. Glatt
- Pacific Brain Health Center, Pacific Neuroscience Institute and Foundation, Santa Monica, CA, USA
| | - Kyron Pierce
- Pacific Brain Health Center, Pacific Neuroscience Institute and Foundation, Santa Monica, CA, USA
| | - Verna R. Porter
- Pacific Brain Health Center, Pacific Neuroscience Institute and Foundation, Santa Monica, CA, USA
- Saint John’s Cancer Institute at Providence Saint John’s Health Center, Santa Monica, CA, USA
- Providence Saint John’s Health Center, Santa Monica, CA, USA
| | - Claudia Wong
- Pacific Brain Health Center, Pacific Neuroscience Institute and Foundation, Santa Monica, CA, USA
- Providence Saint John’s Health Center, Santa Monica, CA, USA
| | - Mihae Kim
- Pacific Brain Health Center, Pacific Neuroscience Institute and Foundation, Santa Monica, CA, USA
- Providence Saint John’s Health Center, Santa Monica, CA, USA
| | - Richelin V. Dye
- Pacific Brain Health Center, Pacific Neuroscience Institute and Foundation, Santa Monica, CA, USA
- Loma Linda University, School of Medicine and School of Behavioral Health, Loma Linda, CA, USA
| | - Stella Panos
- Pacific Brain Health Center, Pacific Neuroscience Institute and Foundation, Santa Monica, CA, USA
| | - Tess Bookheimer
- Pacific Brain Health Center, Pacific Neuroscience Institute and Foundation, Santa Monica, CA, USA
| | - Tori Togashi
- Pacific Brain Health Center, Pacific Neuroscience Institute and Foundation, Santa Monica, CA, USA
- Loma Linda University, School of Medicine and School of Behavioral Health, Loma Linda, CA, USA
| | - Spencer Loong
- Pacific Brain Health Center, Pacific Neuroscience Institute and Foundation, Santa Monica, CA, USA
- Loma Linda University, School of Medicine and School of Behavioral Health, Loma Linda, CA, USA
| | - Cyrus A. Raji
- Pacific Brain Health Center, Pacific Neuroscience Institute and Foundation, Santa Monica, CA, USA
- Mallinckrodt Institute of Radiology, Washington University, St. Louis, MO, USA
| | - Susan Y. Bookheimer
- Pacific Brain Health Center, Pacific Neuroscience Institute and Foundation, Santa Monica, CA, USA
- David Geffen School of Medicine at University of California Los Angeles, Los Angeles, CA, USA
| | | | - David A. Merrill
- Pacific Brain Health Center, Pacific Neuroscience Institute and Foundation, Santa Monica, CA, USA
- Saint John’s Cancer Institute at Providence Saint John’s Health Center, Santa Monica, CA, USA
- Providence Saint John’s Health Center, Santa Monica, CA, USA
- David Geffen School of Medicine at University of California Los Angeles, Los Angeles, CA, USA
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Extra-Virgin Olive Oil Enhances the Blood-Brain Barrier Function in Mild Cognitive Impairment: A Randomized Controlled Trial. Nutrients 2022; 14:nu14235102. [PMID: 36501136 PMCID: PMC9736478 DOI: 10.3390/nu14235102] [Citation(s) in RCA: 30] [Impact Index Per Article: 10.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/15/2022] [Revised: 11/24/2022] [Accepted: 11/28/2022] [Indexed: 12/02/2022] Open
Abstract
Mild cognitive impairment (MCI) and early Alzheimer's disease (AD) are characterized by blood-brain barrier (BBB) breakdown leading to abnormal BBB permeability ahead of brain atrophy or dementia. Previous findings in AD mouse models have reported the beneficial effect of extra-virgin olive oil (EVOO) against AD, which improved BBB and memory functions and reduced brain amyloid-β (Aβ) and related pathology. This work aimed to translate these preclinical findings to humans in individuals with MCI. We examined the effect of daily consumption of refined olive oil (ROO) and EVOO for 6 months in MCI subjects on BBB permeability (assessed by contrast-enhanced MRI), and brain function (assessed using functional-MRI) as the primary outcomes. Cognitive function and AD blood biomarkers were also assessed as the secondary outcomes. Twenty-six participants with MCI were randomized with 25 participants completed the study. EVOO significantly improved clinical dementia rating (CDR) and behavioral scores. EVOO also reduced BBB permeability and enhanced functional connectivity. While ROO consumption did not alter BBB permeability or brain connectivity, it improved CDR scores and increased functional brain activation to a memory task in cortical regions involved in perception and cognition. Moreover, EVOO and ROO significantly reduced blood Aβ42/Aβ40 and p-tau/t-tau ratios, suggesting that both altered the processing and clearance of Aβ. In conclusion, EVOO and ROO improved CDR and behavioral scores; only EVOO enhanced brain connectivity and reduced BBB permeability, suggesting EVOO biophenols contributed to such an effect. This proof-of-concept study justifies further clinical trials to assess olive oil's protective effects against AD and its potential role in preventing MCI conversion to AD and related dementias.
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22
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Kim JW, Byun MS, Yi D, Lee JH, Sung K, Han D, Byeon G, Kim MJ, Jung JH, Chang YY, Jung G, Lee JY, Lee YS, Kim YK, Kang KM, Sohn CH, Lee DY. Association of low meal frequency with decreased in vivo Alzheimer's pathology. iScience 2022; 25:105422. [PMID: 36388975 PMCID: PMC9646955 DOI: 10.1016/j.isci.2022.105422] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/04/2022] [Revised: 09/11/2022] [Accepted: 10/18/2022] [Indexed: 11/06/2022] Open
Abstract
Little is known about the association between meal frequency and Alzheimer's disease (AD) in humans. We tested the hypothesis that low meal frequency (LMF) is associated with reduced in vivo AD pathology in human brain, and additionally investigated the mediation of serum ghrelin, a hunger-related hormone, for the association. A total of 411 non-demented older adults were systematically interviewed to identify their dietary patterns including meal frequency and underwent multi-modal neuroimaging for cerebral beta-amyloid (Aβ) and tau deposition, glucose metabolism, and cerebrovascular injury. LMF (less than three meals a day) was significantly associated with lower Aβ deposition compared to high meal frequency (HMF). In addition, both LMF and reduced Aβ deposition were significantly related to elevated serum ghrelin. Our findings suggest that LMF may be related to the lower risk of AD through reduced brain amyloid deposition. Additionally, ghrelin appears mediate the association between LMF and lower amyloid deposition.
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Affiliation(s)
- Jee Wook Kim
- Department of Neuropsychiatry, Hallym University Dongtan Sacred Heart Hospital, 7 Keunjaebong-gil, Hwaseong, Gyeonggi 18450, Republic of Korea
- Department of Psychiatry, Hallym University College of Medicine, Chuncheon, Gangwon 24252, Republic of Korea
| | - Min Soo Byun
- Department of Psychiatry, Seoul National University College of Medicine, Seoul 03080, Republic of Korea
- Department of Neuropsychiatry, Seoul National University Hospital, Seoul 03080, Republic of Korea
| | - Dahyun Yi
- Medical Research Center Seoul National University, Institute of Human Behavioral Medicine, Seoul 03080, Republic of Korea
| | - Jun Ho Lee
- Department of Neuropsychiatry, Seoul National University Hospital, Seoul 03080, Republic of Korea
| | - Kiyoung Sung
- Department of Psychiatry, Eulji University Nowon Eulji Medical Center, Seoul 01830, Republic of Korea
| | - Dongkyun Han
- Department of Psychiatry, Seoul National University College of Medicine, Seoul 03080, Republic of Korea
| | - Gihwan Byeon
- Department of Neuropsychiatry, Kangwon National University Hospital, Chuncheon 24289, Republic of Korea
| | - Min Jung Kim
- Department of Psychiatry, Eulji University Nowon Eulji Medical Center, Seoul 01830, Republic of Korea
| | - Joon Hyung Jung
- Department of Neuropsychiatry, Seoul National University Hospital, Seoul 03080, Republic of Korea
| | - Yoon Young Chang
- Department of Neuropsychiatry, Seoul National University Hospital, Seoul 03080, Republic of Korea
| | - Gijung Jung
- Department of Neuropsychiatry, Seoul National University Hospital, Seoul 03080, Republic of Korea
| | - Jun-Young Lee
- Department of Neuropsychiatry, SMG-SNU Boramae Medical Center, Seoul 07061, Republic of Korea
| | - Yun-Sang Lee
- Department of Nuclear Medicine, Seoul National University College of Medicine, 101 Daehak-ro, Jongno-gu, Seoul 03080, Republic of Korea
| | - Yu Kyeong Kim
- Department of Nuclear Medicine, SMG-SNU Boramae Medical Center, Seoul 07061, Republic of Korea
| | - Koung Mi Kang
- Department of Radiology, Seoul National University Hospital, Seoul 03080, Republic of Korea
| | - Chul-Ho Sohn
- Department of Radiology, Seoul National University Hospital, Seoul 03080, Republic of Korea
| | - Dong Young Lee
- Department of Psychiatry, Seoul National University College of Medicine, Seoul 03080, Republic of Korea
- Department of Neuropsychiatry, Seoul National University Hospital, Seoul 03080, Republic of Korea
- Medical Research Center Seoul National University, Institute of Human Behavioral Medicine, Seoul 03080, Republic of Korea
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Tussing-Humphreys L, Lamar M, McLeod A, Schiffer L, Blumstein L, Dakers R, Karstens A, Hemphill NON, Strahan D, Siegel L, Flack JS, Antonic M, Restrepo L, Berbaum M, Fitzgibbon M. Effect of Mediterranean diet and Mediterranean diet plus calorie restriction on cognition, lifestyle, and cardiometabolic health: A randomized clinical trial. Prev Med Rep 2022; 29:101955. [PMID: 36161108 PMCID: PMC9502289 DOI: 10.1016/j.pmedr.2022.101955] [Citation(s) in RCA: 7] [Impact Index Per Article: 2.3] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/09/2022] [Revised: 08/06/2022] [Accepted: 08/14/2022] [Indexed: 11/30/2022] Open
Abstract
A Mediterranean diet and intentional weight loss each positively affect cognitive functioning. Combining both could produce synergistic effects on cognition. The purpose of this study is to compare a Mediterranean diet lifestyle intervention with and without caloric restriction versus control on cognition, lifestyle, and cardiometabolic disease. In a three-arm trial conducted between 2017 and 2020 in Chicago, one hundred and eight-five, 55–85-year-old, predominately non-Hispanic black females with obesity were randomized (2:2:1) to an 8-month Mediterranean diet plus caloric restriction intervention, Mediterranean diet alone, or control. The primary outcome was change from baseline to post-intervention in cognitive composite scores: attention, information & processing; executive function; and learning, memory, & recognition. Secondary outcomes were weight, lifestyle and cardiometabolic markers. The 8-month Mediterranean diet interventions did not significantly affect cognition. Adherence to a Mediterranean diet improved more in the Mediterranean diet plus caloric restriction arm (mean [SE] score change, +6.3 [0.7] points) and Mediterranean diet alone arm (+4.8 [0.7] points) relative to controls (+0.6 [0.9] points). Mean weight loss was greater among the Mediterranean diet plus caloric restriction arm (−4.6 [0.6] kg) compared to the Mediterranean diet alone (−2.6 [0.6] kg) and control arms (−0.6 [0.7] kg). The interventions did not affect activity or cardiometabolic risk markers; although, fasting insulin did decline in the Mediterranean diet plus caloric restriction arm relative to the Mediterranean diet alone and control arms. A Mediterranean diet lifestyle intervention with and without caloric restriction did not significantly affect cognitive function compared to controls. The Mediterranean diet interventions, however, significantly affected diet quality and body weight.
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Affiliation(s)
- Lisa Tussing-Humphreys
- Department of Kinesiology and Nutrition, University of Illinois at Chicago, Chicago, IL, USA
- Institute for Health Research and Policy, University of Illinois at Chicago, Chicago, IL, USA
- University of Illinois Cancer Center, University of Illinois Chicago, Chicago, IL, USA
| | - Melissa Lamar
- Department of Psychiatry and Behavioral Sciences, Division of Behavioral Sciences, Rush Medical College, Chicago, IL, USA
| | - Andrew McLeod
- Department of Kinesiology and Nutrition, University of Illinois at Chicago, Chicago, IL, USA
- Institute for Health Research and Policy, University of Illinois at Chicago, Chicago, IL, USA
| | - Linda Schiffer
- Institute for Health Research and Policy, University of Illinois at Chicago, Chicago, IL, USA
| | - Lara Blumstein
- Institute for Health Research and Policy, University of Illinois at Chicago, Chicago, IL, USA
| | - Roxanne Dakers
- Institute for Health Research and Policy, University of Illinois at Chicago, Chicago, IL, USA
| | - Aimee Karstens
- Institute for Health Research and Policy, University of Illinois at Chicago, Chicago, IL, USA
- Mayo Clinic, Rochester, MN, USA
| | - Nefertiti Oji Njideka Hemphill
- Department of Kinesiology and Nutrition, University of Illinois at Chicago, Chicago, IL, USA
- Institute for Health Research and Policy, University of Illinois at Chicago, Chicago, IL, USA
| | - Desmona Strahan
- Institute for Health Research and Policy, University of Illinois at Chicago, Chicago, IL, USA
- Department of Pediatrics, University of Illinois at Chicago, Chicago, IL, USA
| | - Leilah Siegel
- Institute for Health Research and Policy, University of Illinois at Chicago, Chicago, IL, USA
- University of Illinois Extension, University of Illinois at Urbana-Champaign, Urbana, IL, USA
| | - Jennifer Sanchez Flack
- Institute for Health Research and Policy, University of Illinois at Chicago, Chicago, IL, USA
- University of Illinois Cancer Center, University of Illinois Chicago, Chicago, IL, USA
- Department of Pediatrics, University of Illinois at Chicago, Chicago, IL, USA
| | - Mirjana Antonic
- Institute for Health Research and Policy, University of Illinois at Chicago, Chicago, IL, USA
- University of Illinois Cancer Center, University of Illinois Chicago, Chicago, IL, USA
- Department of Pediatrics, University of Illinois at Chicago, Chicago, IL, USA
| | - Leo Restrepo
- Institute for Health Research and Policy, University of Illinois at Chicago, Chicago, IL, USA
| | - Michael Berbaum
- Institute for Health Research and Policy, University of Illinois at Chicago, Chicago, IL, USA
- School of Public Health, University of Illinois at Chicago, Chicago, IL, USA
- Center for Clinical and Translational Science, University of Illinois at Chicago, Chicago, IL, USA
| | - Marian Fitzgibbon
- Institute for Health Research and Policy, University of Illinois at Chicago, Chicago, IL, USA
- University of Illinois Cancer Center, University of Illinois Chicago, Chicago, IL, USA
- Department of Pediatrics, University of Illinois at Chicago, Chicago, IL, USA
- Corresponding author at: University of Illinois at Chicago, 1747 W. Roosevelt Rd. MC 558, Chicago, IL 60608, USA.
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24
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Vassilopoulou E, Koumbi L, Karastogiannidou C, Sotiriadis PM, Felicia PC, Tsolaki M. Adjustment of the MIND diet tool for discriminating Greek patients with dementia: A confirmatory factor analysis. Front Neurol 2022; 13:811314. [PMID: 36188390 PMCID: PMC9516637 DOI: 10.3389/fneur.2022.811314] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/08/2021] [Accepted: 08/09/2022] [Indexed: 12/04/2022] Open
Abstract
BACKGROUND The MIND diet, a hybrid of the Mediterranean and DASH diets, has been shown to reduce cognitive decline and dementia occurrence. AIM In the current cross-sectional study the effect of the MIND diet in elderly Greek individuals, assessed for cognitive decline, was investigated. Confirmatory factor analysis (CFA) evaluated the MIND diet score's factor structure in relation to the ability to distinguish the Greek elderly population diagnosed with or without dementia. METHODS One hundred fifteen participants recently diagnosed with dementia and 52 cognitively healthy controls, after proper neuropsychological testing by neurologists, were included. To ensure the variance-covariance of matrix for the CFA, a second reference group of 36 participants who self-reported as healthy in terms of cognitive status from the general Greek population, was included. Demographic, anthropometric characteristics, emotional status, cognitive function, and dementia diagnosis were recorded. A prediction model investigated the MIND diet's components to separate the study participants according to their cognitive health. CFA was used to examine if the structure of the MIND diet tool scale was a proper model fit or if a different model more appropriately fit our sample data. RESULTS AND DISCUSSION The CFA conducted, suggested that the 9 components MIND diet score supported our sample data better than the original 15-item MIND diet. CONCLUSION The MIND diets' components must be considered in relevance to the dietary habits and cultural background of the respective population studied. Future studies should evaluate prospectively the effect of MIND-9 on preventing the onset of dementia in Greek adults.
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Affiliation(s)
- Emilia Vassilopoulou
- Department of Nutritional Sciences and Dietetics, International Hellenic University, Thessaloniki, Greece
| | - Lemonica Koumbi
- Department of Nutritional Sciences and Dietetics, International Hellenic University, Thessaloniki, Greece
| | - Calliope Karastogiannidou
- Department of Nutritional Sciences and Dietetics, International Hellenic University, Thessaloniki, Greece
| | | | - Pop Claudia Felicia
- Department of Nursing “Iuliu Hatieganu”, Department of Medicine and Pharmacy, University of Medicine and Pharmacy, Cluj-Napoca, Romania
| | - Magda Tsolaki
- 1st Department of Neurology, Aristotle University of Thessaloniki, AHEPA University Hospital, Thessaloniki, Greece
- Greek Alzheimer Association and Related Disorders, Thessaloniki, Greece
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Zhou Y, Wang J, Cao L, Shi M, Liu H, Zhao Y, Xia Y. Fruit and Vegetable Consumption and Cognitive Disorders in Older Adults: A Meta-Analysis of Observational Studies. Front Nutr 2022; 9:871061. [PMID: 35795585 PMCID: PMC9251442 DOI: 10.3389/fnut.2022.871061] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/07/2022] [Accepted: 05/25/2022] [Indexed: 11/13/2022] Open
Abstract
ObjectivesThe aim of this meta-analysis was to assess the quantitative associations between fruit and vegetable intake and cognitive disorders in older adults.DesignA meta-analysis.Setting and ParticipantsWe used the PubMed, Web of Science and Scopus databases for a literature search to 12 April 2022. We preliminarily retrieved 11,759 studies, 16 of which met the inclusion criteria including six cross-sectional studies, nine cohort studies and one case-control study, incorporating 64,348 participants and 9,879 cases.MethodsUsing the three databases, we identified observational studies exploring the association. The pooled odds ratios (ORs) and 95% confidence intervals (CIs) were calculated using a random effects model.ResultsSixteen studies were included in the meta-analysis, and the results showed that increased fruit and vegetable consumption in older adults was associated with a decline in the prevalence of cognitive disorders (OR: 0.79, 95% CI: 0.76–0.83). Moreover, intake of fruits (OR: 0.83, 95% CI: 0.77–0.89) and vegetables (OR: 0.75, 95% CI: 0.70–0.80) alone were both associated with a lower prevalence of cognitive disorders. Subgroup analyses indicated that the intake of fruits and vegetables was associated with the prevalence of cognitive impairment (OR: 0.72, 95% CI: 0.76–0.80) and dementia (OR: 0.84, 95% CI: 0.78–0.91) but not Alzheimer’s disease (OR: 0.88, 95% CI: 0.76–1.01).Conclusion and ImplicationsOur meta-analysis provides evidence that the intake of fruits and vegetables is inversely proportional and linearly associated with the prevalence of cognitive disorders in older adults. Future research is required to further investigate the preventive effects of the frequency, quantity, and duration of eating vegetables and fruits on cognitive disorders in older adults.
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Affiliation(s)
- Yuhan Zhou
- Department of Clinical Epidemiology, Shengjing Hospital of China Medical University, Shenyang, China
| | - Jieyuan Wang
- Tibet Military Region Centers for Disease Control and Prevention of PLA, Tibet, China
| | - Limin Cao
- The Third Central Hospital of Tianjin, Tianjin, China
| | - Mengyuan Shi
- Department of Clinical Epidemiology, Shengjing Hospital of China Medical University, Shenyang, China
| | - Huiyuan Liu
- Department of Clinical Epidemiology, Shengjing Hospital of China Medical University, Shenyang, China
| | - Yuhong Zhao
- Department of Clinical Epidemiology, Shengjing Hospital of China Medical University, Shenyang, China
| | - Yang Xia
- Department of Clinical Epidemiology, Shengjing Hospital of China Medical University, Shenyang, China
- *Correspondence: Yang Xia, ;
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Choe YM, Suh GH, Lee BC, Choi IG, Lee JH, Kim HS, Kim JW. Association Between Copper and Global Cognition and the Moderating Effect of Iron. Front Aging Neurosci 2022; 14:811117. [PMID: 35422696 PMCID: PMC9003994 DOI: 10.3389/fnagi.2022.811117] [Citation(s) in RCA: 9] [Impact Index Per Article: 3.0] [Reference Citation Analysis] [Abstract] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/08/2021] [Accepted: 02/14/2022] [Indexed: 11/13/2022] Open
Abstract
Background Despite the known association between abnormal serum copper levels and Alzheimer’s disease (AD) or cognitive decline, the association between copper, iron, and cognition remains poorly investigated. We examined the association between serum copper levels and global cognition measured using the Mini-Mental State Examination (MMSE) in older adults with normal copper levels. We also explored the moderating effect of iron on this association. Methods The study enrolled 99 non-demented adults between 65 and 90 years of age. All the participants underwent comprehensive clinical assessments and serum copper measurements. Global cognitive performance was measured by the MMSE. All copper levels were within the normal range and were stratified into three categories: < 87 (low), 87–98 (medium), and > 98 (high: used as a reference category) μg/dL. Results Serum copper level (as a continuous variable) was significantly associated with MMSE score (B = 0.065, 95% confidence interval = 0.023–0.108, p = 0.003). Low serum copper group showed significantly decreased MMSE score compared to high copper one (B = −2.643, 95% confidence interval = −4.169 to -1.117, p < 0.001), while middle copper category had no difference (B = −1.211, 95% confidence interval = −2.689 to 0.268, p = 0.107). There was a significant low serum copper ×iron interaction effect on the MMSE score (B = 0.065, 95% confidence interval = 0.016–0.114, p = 0.010). Subgroup analyses showed that low serum copper was significantly associated with a low MMSE score in the low-iron (B = −4.174, 95% confidence interval = −6.607 to −1.741, p = 0.001) but not high-iron subgroup (B = −0.721, 95% confidence interval = −2.852 to 1.409, p = 0.495). Conclusion Our findings from non-demented older adults suggest that a low serum copper level within the normal range was associated with AD or cognitive decline and this is moderated by iron. To prevent AD or cognitive decline, clinicians need to pay attention to avoiding low serum copper and iron levels, even within the clinical normal range.
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Affiliation(s)
- Young Min Choe
- Department of Neuropsychiatry, Hallym University Dongtan Sacred Heart Hospital, Hwaseong, South Korea
- Department of Psychiatry, Hallym University College of Medicine, Chuncheon, South Korea
| | - Guk-Hee Suh
- Department of Neuropsychiatry, Hallym University Dongtan Sacred Heart Hospital, Hwaseong, South Korea
- Department of Psychiatry, Hallym University College of Medicine, Chuncheon, South Korea
| | - Boung Chul Lee
- Department of Psychiatry, Hallym University College of Medicine, Chuncheon, South Korea
- Department of Neuropsychiatry, Hallym University Hangang Sacred Heart Hospital, Seoul, South Korea
| | - Ihn-Geun Choi
- Department of Psychiatry, Hallym University College of Medicine, Chuncheon, South Korea
- Department of Psychiatry, Seoul W Psychiatric Office, Seoul, South Korea
| | - Jun Ho Lee
- Department of Neuropsychiatry, Seoul National University Hospital, Seoul, South Korea
| | - Hyun Soo Kim
- Department of Laboratory Medicine, Hallym University Dongtan Sacred Heart Hospital, Hwaseong, South Korea
| | - Jee Wook Kim
- Department of Neuropsychiatry, Hallym University Dongtan Sacred Heart Hospital, Hwaseong, South Korea
- Department of Psychiatry, Hallym University College of Medicine, Chuncheon, South Korea
- *Correspondence: Jee Wook Kim,
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Long-term association of vegetable and fruit intake with risk of dementia in Japanese older adults: the Hisayama study. BMC Geriatr 2022; 22:257. [PMID: 35351024 PMCID: PMC8962464 DOI: 10.1186/s12877-022-02939-2] [Citation(s) in RCA: 19] [Impact Index Per Article: 6.3] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/08/2021] [Accepted: 03/10/2022] [Indexed: 11/10/2022] Open
Abstract
Abstract
Background
Several prospective Western studies have reported an inverse association of vegetable and fruit intake with dementia risk. However, there is limited epidemiologic evidence in Asians. This study investigated the association of intakes of vegetables, fruits, and their nutrients on the risk of incident dementia and its subtypes in a Japanese community.
Methods
A total of 1071 participants (452 men and 619 women) aged ≥60 years without dementia at baseline were prospectively followed up for 24 years. Intakes of vegetables, fruits, and nutrients were evaluated using a 70-item semiquantitative food frequency questionnaire at baseline and were categorized into quartiles separately by gender. The outcome measure was the development of dementia and its subtypes—namely, Alzheimer’s disease (AD) and vascular dementia (VaD). The risk estimates of incident dementia were computed using a Cox proportional hazards model.
Results
During the long-term follow-up period, 464 subjects developed dementia, of whom 286 had AD and 144 had VaD. Higher vegetable intake was associated gradually with lower risk of developing dementia and AD (both P-trend < 0.05), but not VaD, after adjusting for confounders. Subjects allocated the highest quartile of vegetable intake had 27 and 31% lower risk of dementia and AD, respectively, than those with the lowest quartile. The risk of dementia decreased significantly with higher intakes of vitamin A, riboflavin, vitamin C, magnesium, calcium, and potassium (all P-trend < 0.05). Subjects with higher total dietary fiber intake tended to be at decreased risk for total dementia (P-trend = 0.07). Meanwhile, there were no significant associations between fruit intake and the risk of dementia and its subtypes.
Conclusion
Higher intakes of vegetables and their constituent nutrients were associated with a lower risk of dementia in Japanese older adults. A diet rich in vegetables may be beneficial in reducing the dementia risk in Asians.
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Larnyo E, Dai B, Nutakor JA, Ampon-Wireko S, Larnyo A, Appiah R. Examining the impact of socioeconomic status, demographic characteristics, lifestyle and other risk factors on adults' cognitive functioning in developing countries: an analysis of five selected WHO SAGE Wave 1 Countries. Int J Equity Health 2022; 21:31. [PMID: 35216605 PMCID: PMC8876754 DOI: 10.1186/s12939-022-01622-7] [Citation(s) in RCA: 8] [Impact Index Per Article: 2.7] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/14/2021] [Accepted: 01/24/2022] [Indexed: 12/15/2022] Open
Abstract
BACKGROUND Though extensive studies have been conducted on assessing the predictors of cognitive functioning among older adults in small community-based samples, very few studies have focused on understanding the impact of socioeconomic status (SES), demographic characteristics and other risk factors such as lifestyle and chronic diseases on the cognitive functioning among adults of all ages in a nationally representative population-based sample across low- and middle-income countries. This study, therefore, seeks to evaluate the impact of SES, demographic characteristics and risk factors on the cognitive functioning of adults across all ages in five selected developing countries. METHODS Data from 12,430 observations obtained from the WHO Study on Global AGEing and Adult Health (SAGE) Wave 1; consisting of 2,486 observations each for China, Ghana, India, the Russian Federation, and South Africa, were used for the study. A meta-regression and a five-step hierarchical linear regression were used to analyze the data, with cognitive functioning as the dependent variable. Independent variables used in this study include SES; assessed by household income and education, demographic characteristics, other risk factors such as lifestyle, self-reported memory difficulty and chronic diseases. RESULTS This study found that SES and lifestyle significantly predicted cognitive functioning in all the five selected countries as obtained by the pooled results of the meta-regression analysis. The hierarchical linear regression results also revealed that demographic characteristics such as age, type of residency, and self-reported memory difficulty significantly impact cognitive functioning in China, Ghana, Russia, and South Africa. CONCLUSION The findings in this study provide new insights for policymakers, caregivers, parents, and individuals, especially those in developing countries, to implement policies and actions targeted at improving SES and eliminating risk factors associated with cognitive decline, as these measures could help improve the cognitive functioning among their populations.
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Affiliation(s)
- Ebenezer Larnyo
- Department of Health Policy and Management, School of Management, Jiangsu University, 301# Xuefu Road, Zhenjiang, 212013, Jiangsu Province, China
| | - Baozhen Dai
- Department of Health Policy and Management, School of Management, Jiangsu University, 301# Xuefu Road, Zhenjiang, 212013, Jiangsu Province, China.
- Department of Labor and Social Security, School of Public Health, Southeast University, 87# Dingjiaqiao, Nanjing, 210009, Jiangsu province, China.
| | - Jonathan Aseye Nutakor
- Department of Health Policy and Management, School of Management, Jiangsu University, 301# Xuefu Road, Zhenjiang, 212013, Jiangsu Province, China
| | - Sabina Ampon-Wireko
- Department of Health Policy and Management, School of Management, Jiangsu University, 301# Xuefu Road, Zhenjiang, 212013, Jiangsu Province, China
| | - Abigail Larnyo
- School of Management, Jiangsu University, 301# Xuefu Road, Zhenjiang, 212013, Jiangsu Province, China
| | - Ruth Appiah
- Department of Health Policy and Management, School of Management, Jiangsu University, 301# Xuefu Road, Zhenjiang, 212013, Jiangsu Province, China
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Subjective cognitive decline and total energy intake: Talk too much? Eur J Epidemiol 2022; 37:129-131. [PMID: 35211870 DOI: 10.1007/s10654-022-00849-6] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/31/2022] [Accepted: 02/01/2022] [Indexed: 11/03/2022]
Abstract
The increasing longevity of the population has resulted in dementia becoming a leading cause of both death and disability. Dementia is not a single disease. Studies of rare Mendelian disorders have documented that Alzheimer's disease, the most common cause of dementia, is associated with a long incubation period from amyloid deposition to neurodegeneration to mild cognitive impairment and dementia. There are three broad hypotheses related to the causes of Alzheimer's dementia: (1) an aging process; (2) brain vascular disease; and (3) metabolic abnormalities associated with either increased production of amyloid-β or decreased clearance from the brain. Therefore, research on the early stages of the dementia process are of high priority. This paper reports that higher energy intake in both the Nurses' Health Study and Health Professionals Follow-up Study is associated with very early symptoms that lead to mild cognitive impairment and dementia. The results are very interesting but hard to interpret because they also show that higher energy intake is not related to body mass index, a very unusual observation. A likely hypothesis is that there is an association between reporting of dietary intake and subjective symptoms, i.e. reporting bias, accounting for their results.
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30
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Carneiro L, Pellerin L. Nutritional Impact on Metabolic Homeostasis and Brain Health. Front Neurosci 2022; 15:767405. [PMID: 35153657 PMCID: PMC8829049 DOI: 10.3389/fnins.2021.767405] [Citation(s) in RCA: 14] [Impact Index Per Article: 4.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/30/2021] [Accepted: 12/13/2021] [Indexed: 12/18/2022] Open
Abstract
Aging in modern societies is often associated with various diseases including metabolic and neurodegenerative disorders. In recent years, researchers have shown that both dysfunctions are related to each other. Although the relationship is not fully understood, recent evidence indicate that metabolic control plays a determinant role in neural defects onset. Indeed, energy balance dysregulation affects neuroenergetics by altering energy supply and thus neuronal activity. Consistently, different diets to help control body weight, blood glucose or insulin sensitivity are also effective in improving neurodegenerative disorders, dampening symptoms, or decreasing the risk of disease onset. Moreover, adapted nutritional recommendations improve learning, memory, and mood in healthy subjects as well. Interestingly, adjusted carbohydrate content of meals is the most efficient for both brain function and metabolic regulation improvement. Notably, documented neurological disorders impacted by specific diets suggest that the processes involved are inflammation, mitochondrial function and redox balance as well as ATP production. Interestingly, processes involving inflammation, mitochondrial function and redox balance as well as ATP production are also described in brain regulation of energy homeostasis. Therefore, it is likely that changes in brain function induced by diets can affect brain control of energy homeostasis and other brain functions such as memory, anxiety, social behavior, or motor skills. Moreover, a defect in energy supply could participate to the development of neurodegenerative disorders. Among the possible processes involved, the role of ketone bodies metabolism, neurogenesis and synaptic plasticity, oxidative stress and inflammation or epigenetic regulations as well as gut-brain axis and SCFA have been proposed in the literature. Therefore, the goal of this review is to provide hints about how nutritional studies could help to better understand the tight relationship between metabolic balance, brain activity and aging. Altogether, diets that help maintaining a metabolic balance could be key to both maintain energy homeostasis and prevent neurological disorders, thus contributing to promote healthy aging.
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Affiliation(s)
- Lionel Carneiro
- Department of Biological Chemistry and Pharmacology, Ohio State University, Columbus, OH, United States
| | - Luc Pellerin
- Inserm U1082, Université de Poitiers and CHU de Poitiers, Poitiers, France
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31
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Neuffer J, Gourru M, Thomas A, Lefèvre-Arbogast S, Foubert-Samier A, Helmer C, Delcourt C, Féart C, Samieri C. A Biological Index to Screen Multi-Micronutrient Deficiencies Associated with the Risk to Develop Dementia in Older Persons from the Community. J Alzheimers Dis 2021; 85:331-342. [PMID: 34806604 DOI: 10.3233/jad-215011] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/17/2022]
Abstract
BACKGROUND Low blood status in several nutritional compounds, including long-chain omega-3 fatty acids (LC n-3 PUFA), carotenoids, and vitamin D, have been associated with a higher risk to develop dementia. Nutritional deficiencies may potentiate each other regarding dementia risk; yet the association of multiple nutritional deficiencies with dementia has been little explored. OBJECTIVE To develop an index of micronutritional biological status (MNBS) for the screening of multi-micronutritional deficiencies associated with the risk of dementia in a prospective population-based cohort of older persons. METHODS We included participants from the Bordeaux Three-City study, who were free of dementia at baseline, had blood measurements of LC n-3 PUFA, carotenoids, and 25(OH)D, and who were followed for up to 18 years for dementia. We used penalized splines in Cox models to model dose-response relationships of each nutritional component with the risk of dementia and construct a risk index. RESULTS 629 participants with an average age of 73.1 years were included in the study. Each increase of 1 SD of the MNBS index was associated with a 46%higher risk of dementia (HR = 1.46, 95%CI 1.23; 1.73). Participants with highest index ([mean+1SD; max]) had a 4-fold increased risk of dementia compared with participants with a low index ([min; mean-1SD]) (HR = 4.17, 95%CI 2.30; 7.57). CONCLUSION This index of assessment of micronutritional biological status is a practical tool that may help identify populations with inadequate nutritional status, screen eligible individuals for nutritional prevention in primary care, or for supplementation in preventive trials of dementia.
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Affiliation(s)
- Jeanne Neuffer
- University of Bordeaux, INSERM, Bordeaux Population Health Research Center, UMR 1219, Bordeaux, France
| | - Marjorie Gourru
- University of Bordeaux, INSERM, Bordeaux Population Health Research Center, UMR 1219, Bordeaux, France
| | - Aline Thomas
- University of Bordeaux, INSERM, Bordeaux Population Health Research Center, UMR 1219, Bordeaux, France
| | - Sophie Lefèvre-Arbogast
- University of Bordeaux, INSERM, Bordeaux Population Health Research Center, UMR 1219, Bordeaux, France
| | | | - Catherine Helmer
- University of Bordeaux, INSERM, Bordeaux Population Health Research Center, UMR 1219, Bordeaux, France
| | - Cécile Delcourt
- University of Bordeaux, INSERM, Bordeaux Population Health Research Center, UMR 1219, Bordeaux, France
| | - Catherine Féart
- University of Bordeaux, INSERM, Bordeaux Population Health Research Center, UMR 1219, Bordeaux, France
| | - Cécilia Samieri
- University of Bordeaux, INSERM, Bordeaux Population Health Research Center, UMR 1219, Bordeaux, France
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32
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Samieri C, Yassine HN, Melo van Lent D, Lefèvre-Arbogast S, van de Rest O, Bowman GL, Scarmeas N. Personalized nutrition for dementia prevention. Alzheimers Dement 2021; 18:1424-1437. [PMID: 34757699 DOI: 10.1002/alz.12486] [Citation(s) in RCA: 22] [Impact Index Per Article: 5.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/16/2021] [Revised: 08/26/2021] [Accepted: 08/30/2021] [Indexed: 12/17/2022]
Abstract
The role of nutrition has been investigated for decades under the assumption of one-size-fits-all. Yet there is heterogeneity in metabolic and neurobiological responses to diet. Thus a more personalized approach may better fit biological reality and have increased efficacy to prevent dementia. Personalized nutrition builds on the food exposome, defined as the history of diet-related exposures over the lifetime, and on its interactions with the genome and other biological characteristics (eg, metabolism, the microbiome) to shape health. We review current advances of personalized nutrition in dementia research. We discuss key questions, success milestones, and future roadmap from observational epidemiology to clinical studies through basic science. A personalized nutrition approach based on the best prescription for the most appropriate target population in the most relevant time-window has the potential to strengthen dementia-prevention efforts.
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Affiliation(s)
- Cécilia Samieri
- Univ. Bordeaux, ISPED, Inserm, Bordeaux Population Health Research Center, Bordeaux, France
| | - Hussein N Yassine
- Department of Medicine, Keck School of Medicine USC, Los Angeles, California, USA.,Department of Neurology, Keck School of Medicine USC, Los Angeles, California, USA
| | - Debora Melo van Lent
- Glenn Biggs Institute for Alzheimer's and Neurodegenerative Diseases, UT Health San Antonio, San Antonio, Texas, USA.,Department of Neurology, Boston University School of Medicine, Boston, Massachusetts, USA
| | | | - Ondine van de Rest
- Division of Human Nutrition and Health, Wageningen University and Research, Wageningen, the Netherlands
| | - Gene L Bowman
- Department of Neurology and Layton Aging and Alzheimer's Disease Center, Oregon Health and Science University, Portland, Oregon, USA.,Helfgott Research Institute, National University of Natural Medicine, Portland, Oregon, USA
| | - Nikolaos Scarmeas
- 1st Department of Neurology, Aiginition Hospital, National and Kapodistrian University of Athens Medical School, Athens, Greece.,Taub Institute for Research in Alzheimer's Disease and the Aging Brain, The Gertrude H. Sergievsky Center, Department of Neurology, Columbia University, New York, New York, USA
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33
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Liu YH, Gao X, Na M, Kris-Etherton PM, Mitchell DC, Jensen GL. Dietary Pattern, Diet Quality, and Dementia: A Systematic Review and Meta-Analysis of Prospective Cohort Studies. J Alzheimers Dis 2021; 78:151-168. [PMID: 32955461 DOI: 10.3233/jad-200499] [Citation(s) in RCA: 45] [Impact Index Per Article: 11.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/28/2023]
Abstract
BACKGROUND Diet is an important lifestyle factor that may prevent or slow the onset and progression of neurodegeneration. Some, but not all, recent studies have suggested that adherence to a healthy dietary pattern may be associated with reduced risk of dementia. OBJECTIVE In this meta-analysis, we systematically examined the associations between overall dietary patterns, assessed a priori and a posteriori, and risk of dementia. METHODS We systematically searched PubMed, Web of Science, and the Cumulative Index for Nursing and Allied Health databases from January 1, 1981 to September 11, 2019. Prospective studies published in English were included. Random-effects model was used to calculate the pooled risk ratios and 95% confidence intervals (CIs). RESULTS Sixteen research articles were identified in the systematic review and 12 research articles including 66,930 participants were further included for the meta-analysis. Adherence to high diet quality or a healthy dietary pattern was significantly associated with lower risk of overall dementia (pooled risk ratio = 0.82; 95% CI: 0.70, 0.95; n = 12) and Alzheimer's disease (pooled risk ratio = 0.61; 95% CI: 0.47, 0.79; n = 6) relative to those with low diet quality or an unhealthy dietary pattern. Subgroup analyses stratified by age, sex, follow-up duration, diet quality assessment approach, study location, and study quality generated similar results. CONCLUSION Adherence to a healthy dietary pattern was associated with lower risk of overall dementia. Further randomized controlled trials are needed to provide additional evidence about the role of a healthy diet on the development and progression of dementia.
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Affiliation(s)
- Yi-Hsuan Liu
- Department of Nutritional Sciences, The Pennsylvania State University, University Park, PA, USA
| | - Xiang Gao
- Department of Nutritional Sciences, The Pennsylvania State University, University Park, PA, USA
| | - Muzi Na
- Department of Nutritional Sciences, The Pennsylvania State University, University Park, PA, USA
| | - Penny M Kris-Etherton
- Department of Nutritional Sciences, The Pennsylvania State University, University Park, PA, USA
| | - Diane C Mitchell
- Department of Nutritional Sciences, The Pennsylvania State University, University Park, PA, USA
| | - Gordon L Jensen
- Larner College of Medicine, University of Vermont, Burlington, VT, USA
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34
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Reveglia P, Paolillo C, Ferretti G, De Carlo A, Angiolillo A, Nasso R, Caputo M, Matrone C, Di Costanzo A, Corso G. Challenges in LC-MS-based metabolomics for Alzheimer's disease early detection: targeted approaches versus untargeted approaches. Metabolomics 2021; 17:78. [PMID: 34453619 PMCID: PMC8403122 DOI: 10.1007/s11306-021-01828-w] [Citation(s) in RCA: 24] [Impact Index Per Article: 6.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 01/30/2021] [Accepted: 08/06/2021] [Indexed: 01/22/2023]
Abstract
BACKGROUND Alzheimer's disease (AD) is one of the most common causes of dementia in old people. Neuronal deficits such as loss of memory, language and problem-solving are severely compromised in affected patients. The molecular features of AD are Aβ deposits in plaques or in oligomeric structures and neurofibrillary tau tangles in brain. However, the challenge is that Aβ is only one piece of the puzzle, and recent findings continue to support the hypothesis that their presence is not sufficient to predict decline along the AD outcome. In this regard, metabolomic-based techniques are acquiring a growing interest for either the early diagnosis of diseases or the therapy monitoring. Mass spectrometry is one the most common analytical platforms used for detection, quantification, and characterization of metabolic biomarkers. In the past years, both targeted and untargeted strategies have been applied to identify possible interesting compounds. AIM OF REVIEW The overall goal of this review is to guide the reader through the most recent studies in which LC-MS-based metabolomics has been proposed as a powerful tool for the identification of new diagnostic biomarkers in AD. To this aim, herein studies spanning the period 2009-2020 have been reported. Advantages and disadvantages of targeted vs untargeted metabolomic approaches have been outlined and critically discussed.
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Affiliation(s)
- Pierluigi Reveglia
- Department of Clinical and Experimental Medicine, University of Foggia, 71122, Foggia, Italy
| | - Carmela Paolillo
- Department of Clinical and Experimental Medicine, University of Foggia, 71122, Foggia, Italy
| | - Gabriella Ferretti
- Department of Neuroscience, School of Medicine, University of Naples Federico II, 80131, Napoli, Italy
| | - Armando De Carlo
- Department of Clinical and Experimental Medicine, University of Foggia, 71122, Foggia, Italy
- Policlinico Riuniti University Hospital, 71122, Foggia, Italy
| | - Antonella Angiolillo
- Department of Medicine and Health Sciences, Center for Research and Training in Aging Medicine, University of Molise, 86100, Campobasso, Italy
| | - Rosarita Nasso
- Department of Neuroscience, School of Medicine, University of Naples Federico II, 80131, Napoli, Italy
| | - Mafalda Caputo
- Department of Molecular Medicine and Medical Biotechnology, School of Medicine, University of Naples Federico II, 80131, Napoli, Italy
| | - Carmela Matrone
- Department of Neuroscience, School of Medicine, University of Naples Federico II, 80131, Napoli, Italy
| | - Alfonso Di Costanzo
- Department of Medicine and Health Sciences, Center for Research and Training in Aging Medicine, University of Molise, 86100, Campobasso, Italy
| | - Gaetano Corso
- Department of Clinical and Experimental Medicine, University of Foggia, 71122, Foggia, Italy.
- Policlinico Riuniti University Hospital, 71122, Foggia, Italy.
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Aoki S, Yamagishi K, Maruyama K, Kishida R, Ikeda A, Umesawa M, Renzhe C, Kubota Y, Hayama-Terada M, Shimizu Y, Muraki I, Imano H, Sankai T, Okada T, Kitamura A, Kiyama M, Iso H. Dietary intake of tocopherols and risk of incident disabling dementia. Sci Rep 2021; 11:16429. [PMID: 34385499 PMCID: PMC8361201 DOI: 10.1038/s41598-021-95671-7] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/12/2020] [Accepted: 07/27/2021] [Indexed: 11/09/2022] Open
Abstract
Tocopherols, strong antioxidants, may be useful in preventing dementia, but the epidemiological evidence is insufficient. We performed a community-based follow-up study of Japanese, the Circulatory Risk in Community Study, involving 3739 people aged 40-64 years at baseline (1985-1999). Incident disabling dementia was followed up from 1999 through 2020. For subtype analysis, we classified disabling dementia into that with and that without a history of stroke. Dietary intake of tocopherols (total, α, β, γ, and δ) were estimated using 24-h recall surveys. During a median follow-up of 19.7 years, 670 cases of disabling dementia developed. Total tocopherol intake was inversely associated with risk of disabling dementia with multivariable hazard ratios (95% confidence intervals) of 0.79 (0.63-1.00) for the highest versus lowest quartiles of total tocopherol intake (P for trend = 0.05). However, the association was strengthened when further adjusted for α-linolenic acid intake (Spearman correlation with total tocopherol intake = 0.93), with multivariable hazard ratios of 0.50 (0.34-0.74) (P for trend = 0.001) but was weakened and nonsignificant when further adjusted for linoleic acid intake (Spearman correlation with total tocopherol intake = 0.92), with multivariable hazard ratios of 0.69 (0.47-1.01) (P for trend = 0.05). Similar but nonsignificant inverse associations were observed for α-, γ-, and δ-tocopherols but not for β-tocopherol. These results were similar regardless of the presence of a history of stroke. Dietary tocopherol intake was inversely associated with risk of disabling dementia, but its independent effect was uncertain owing to a high intercorrelation of α-linolenic linoleic acids with total tocopherol intake. Even with such confounding, a diet high in tocopherols may help prevent the onset of dementia.
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Affiliation(s)
- Shoko Aoki
- Department of Public Health Medicine, Faculty of Medicine, and Health Services Research and Development Center, University of Tsukuba, Tennodai 1-1-1, Tsukuba, 305-8575, Japan
| | - Kazumasa Yamagishi
- Department of Public Health Medicine, Faculty of Medicine, and Health Services Research and Development Center, University of Tsukuba, Tennodai 1-1-1, Tsukuba, 305-8575, Japan. .,Osaka Center for Cancer and Cardiovascular Disease Prevention, Osaka, Japan. .,Ibaraki Western Medical Center, Chikusei, Japan.
| | - Koutatsu Maruyama
- Department of Bioscience, Graduate School of Agriculture, Ehime University, Matsuyama, Japan
| | - Rie Kishida
- Department of Public Health Medicine, Faculty of Medicine, and Health Services Research and Development Center, University of Tsukuba, Tennodai 1-1-1, Tsukuba, 305-8575, Japan
| | - Ai Ikeda
- Department of Public Health, Juntendo University, Tokyo, Japan
| | - Mitsumasa Umesawa
- Department of Public Health Medicine, Faculty of Medicine, and Health Services Research and Development Center, University of Tsukuba, Tennodai 1-1-1, Tsukuba, 305-8575, Japan.,Department of Public Health, Dokkyo Medical University, Mibu, Japan
| | - Cui Renzhe
- Public Health, Department of Social Medicine, Osaka University Graduate School of Medicine, Suita, Japan
| | - Yasuhiko Kubota
- Osaka Center for Cancer and Cardiovascular Disease Prevention, Osaka, Japan
| | - Mina Hayama-Terada
- Osaka Center for Cancer and Cardiovascular Disease Prevention, Osaka, Japan.,Yao City Public Health Center, Yao, Japan
| | - Yuji Shimizu
- Osaka Center for Cancer and Cardiovascular Disease Prevention, Osaka, Japan
| | - Isao Muraki
- Public Health, Department of Social Medicine, Osaka University Graduate School of Medicine, Suita, Japan
| | - Hironori Imano
- Public Health, Department of Social Medicine, Osaka University Graduate School of Medicine, Suita, Japan
| | - Tomoko Sankai
- Department of Public Health and Nursing, Faculty of Medicine, University of Tsukuba, Tsukuba, Japan
| | - Takeo Okada
- Osaka Center for Cancer and Cardiovascular Disease Prevention, Osaka, Japan
| | - Akihiko Kitamura
- Osaka Center for Cancer and Cardiovascular Disease Prevention, Osaka, Japan.,Research Team for Social Participation and Community Health, Tokyo Metropolitan Institute of Gerontology, Tokyo, Japan
| | - Masahiko Kiyama
- Osaka Center for Cancer and Cardiovascular Disease Prevention, Osaka, Japan
| | - Hiroyasu Iso
- Department of Public Health Medicine, Faculty of Medicine, and Health Services Research and Development Center, University of Tsukuba, Tennodai 1-1-1, Tsukuba, 305-8575, Japan.,Public Health, Department of Social Medicine, Osaka University Graduate School of Medicine, Suita, Japan
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Tanprasertsuk J, Scott TM, Barbey AK, Barger K, Wang XD, Johnson MA, Poon LW, Vishwanathan R, Matthan NR, Lichtenstein AH, Ferland G, Johnson EJ. Carotenoid-Rich Brain Nutrient Pattern Is Positively Correlated With Higher Cognition and Lower Depression in the Oldest Old With No Dementia. Front Nutr 2021; 8:704691. [PMID: 34268331 PMCID: PMC8275828 DOI: 10.3389/fnut.2021.704691] [Citation(s) in RCA: 4] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/03/2021] [Accepted: 05/31/2021] [Indexed: 12/17/2022] Open
Abstract
Background: Healthy dietary patterns are related to better cognitive health in aging populations. While levels of individual nutrients in neural tissues are individually associated with cognitive function, the investigation of nutrient patterns in human brain tissue has not been conducted. Methods: Brain tissues were acquired from frontal and temporal cortices of 47 centenarians from the Georgia Centenarian Study. Fat-soluble nutrients (carotenoids, vitamins A, E, K, and fatty acids [FA]) were measured and averaged from the two brain regions. Nutrient patterns were constructed using principal component analysis. Cognitive composite scores were constructed from cognitive assessment from the time point closest to death. Dementia status was rated by Global Deterioration Scale (GDS). Pearson's correlation coefficients between NP scores and cognitive composite scores were calculated controlling for sex, education, hypertension, diabetes, and APOE ε4 allele. Result: Among non-demented subjects (GDS = 1-3, n = 23), a nutrient pattern higher in carotenoids was consistently associated with better performance on global cognition (r = 0.38, p = 0.070), memory (r = 0.38, p = 0.073), language (r = 0.42, p = 0.046), and lower depression (r = -0.40, p = 0.090). The findings were confirmed with univariate analysis. Conclusion: Both multivariate and univariate analyses demonstrate that brain nutrient pattern explained mainly by carotenoid concentrations is correlated with cognitive function among subjects who had no dementia. Investigation of their synergistic roles on the prevention of age-related cognitive impairment remains to be performed.
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Affiliation(s)
- Jirayu Tanprasertsuk
- Gerald J. and Dorothy R. Friedman School of Nutrition Science and Policy, Tufts University, Boston, MA, United States
| | - Tammy M. Scott
- Gerald J. and Dorothy R. Friedman School of Nutrition Science and Policy, Tufts University, Boston, MA, United States
| | - Aron K. Barbey
- Department of Psychology, Beckman Institute for Advanced Science and Technology, University of Illinois at Urbana-Champaign, Urbana, IL, United States
| | - Kathryn Barger
- Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, Boston, MA, United States
| | - Xiang-Dong Wang
- Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, Boston, MA, United States
| | - Mary Ann Johnson
- Department of Nutrition and Health Sciences, University of Nebraska Lincoln, Lincoln, NE, United States
| | - Leonard W. Poon
- Institute of Gerontology, College of Public Health, University of Georgia, Athens, GA, United States
| | - Rohini Vishwanathan
- Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, Boston, MA, United States
| | - Nirupa R. Matthan
- Gerald J. and Dorothy R. Friedman School of Nutrition Science and Policy, Tufts University, Boston, MA, United States
- Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, Boston, MA, United States
| | - Alice H. Lichtenstein
- Gerald J. and Dorothy R. Friedman School of Nutrition Science and Policy, Tufts University, Boston, MA, United States
- Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, Boston, MA, United States
| | - Guylaine Ferland
- Département de Nutrition, Université de Montréal, Montréal, QC, Canada
| | - Elizabeth J. Johnson
- Gerald J. and Dorothy R. Friedman School of Nutrition Science and Policy, Tufts University, Boston, MA, United States
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Manippa V. RE: Italian breakfast in mind: The effect of caffeine, carbohydrate and protein on physiological state, mood and cognitive performance. Physiol Behav 2021; 237:113462. [PMID: 33992666 DOI: 10.1016/j.physbeh.2021.113462] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/26/2022]
Affiliation(s)
- Valerio Manippa
- Department of Psychological, Health and Territorial Sciences, University G. "d'Annunzio" of Chieti-Pescara, Chieti, Italy.
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38
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Malik A, Ramadan A, Vemuri B, Siddiq W, Amangurbanova M, Ali A, Welty FK. ω-3 Ethyl ester results in better cognitive function at 12 and 30 months than control in cognitively healthy subjects with coronary artery disease: a secondary analysis of a randomized clinical trial. Am J Clin Nutr 2021; 113:1168-1176. [PMID: 33675344 PMCID: PMC8243604 DOI: 10.1093/ajcn/nqaa420] [Citation(s) in RCA: 17] [Impact Index Per Article: 4.3] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/26/2020] [Accepted: 12/11/2020] [Indexed: 11/14/2022] Open
Abstract
BACKGROUND Omega-3 (n-3) fatty acids have shown benefit in cognitively impaired subjects, but the effect on cognitively healthy older subjects is unclear. OBJECTIVES Our aim was to determine if long-term, high-dose ω-3 ethyl esters, EPA (20:5n-3) and DHA (22:6n-3), prevent deterioration of cognitive function in cognitively healthy older adults. METHODS A total of 285 subjects with stable coronary artery disease (CAD) on statin treatment were randomly assigned to 3.36 g EPA and DHA or none (control) for 30 mo. Cognitive function was assessed in all 285 subjects at baseline and in 268 and 250 subjects who returned at 12- and 30-mo follow-up, respectively, with neuropsychological testing as a prespecified secondary outcome. A completer's analysis, along with a sensitivity analysis carrying forward the last observation, was performed. RESULTS Over the 30-mo period, subjects randomly assigned to EPA and DHA had significantly better scores than control for verbal fluency, language, and memory (mean: 1.08; 95% CI: 0.25, 1.91; P = 0.011) and 2 tests of visual-motor coordination (mean: -2.95; 95% CI: -5.33, -0.57; P = 0.015 and mean: -9.44; 95% CI: -18.60, -0.30; P = 0.043, respectively). The better scores for EPA and DHA were due to an improvement at 12 mo compared with baseline in verbal fluency, language, and memory (P = 0.047) and 2 tests of visual-motor coordination (P = 0.033 and P < 0.001, respectively), whereas control had no change. Post hoc analyses indicated no difference by age, sex, or diabetes status. CONCLUSIONS Cognitively healthy older adults with stable CAD randomly assigned to high-dose EPA and DHA had improved cognitive function over a 30-mo period compared with control. These findings may be especially important for CAD patients because CAD is a risk factor for cognitive decline.This trial was registered at clinicaltrials.gov as NCT01624727.
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Affiliation(s)
- Abdulaziz Malik
- Division of Cardiovascular Medicine, Beth Israel Deaconess
Medical Center, Harvard Medical School, Boston, MA,
USA
| | - Amira Ramadan
- Division of Cardiovascular Medicine, Beth Israel Deaconess
Medical Center, Harvard Medical School, Boston, MA,
USA
| | - Bhavya Vemuri
- Division of Cardiovascular Medicine, Beth Israel Deaconess
Medical Center, Harvard Medical School, Boston, MA,
USA
| | - Wardah Siddiq
- Division of Cardiovascular Medicine, Beth Israel Deaconess
Medical Center, Harvard Medical School, Boston, MA,
USA
| | - Maral Amangurbanova
- Division of Cardiovascular Medicine, Beth Israel Deaconess
Medical Center, Harvard Medical School, Boston, MA,
USA
| | - Aamir Ali
- Division of Cardiovascular Medicine, Beth Israel Deaconess
Medical Center, Harvard Medical School, Boston, MA,
USA
| | - Francine K Welty
- Division of Cardiovascular Medicine, Beth Israel Deaconess
Medical Center, Harvard Medical School, Boston, MA,
USA
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Muñoz-Garach A, Cornejo-Pareja I, Martínez-González MÁ, Bulló M, Corella D, Castañer O, Romaguera D, Vioque J, Alonso-Gómez ÁM, Wärnberg J, Martínez JA, Serra-Majem L, Estruch R, Bernal-López MR, Lapetra J, Pintó X, Tur JA, López-Miranda J, Bueno-Cavanillas A, Delgado-Rodríguez M, Matía-Martín P, Daimiel L, Sánchez VM, Vidal J, Prieto L, Ros E, Fernández-Aranda F, Camacho-Barcia L, Ortega-Azorin C, Soria M, Fiol M, Compañ-Gabucio L, Goicolea-Güemez L, Pérez-López J, Goñi N, Pérez-Cabrera J, Sacanella E, Fernández-García JC, Miró-Moriano L, Gimenez-Gracia M, Razquin C, Paz-Graniel I, Guillem P, Zomeño MD, Moñino M, Oncina-Canovas A, Salaverria-Lete I, Toledo E, Salas-Salvadó J, Schröder H, Tinahones FJ. Milk and Dairy Products Intake Is Related to Cognitive Impairment at Baseline in Predimed Plus Trial. Mol Nutr Food Res 2021; 65:e2000728. [PMID: 33471961 DOI: 10.1002/mnfr.202000728] [Citation(s) in RCA: 10] [Impact Index Per Article: 2.5] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/23/2020] [Revised: 12/30/2020] [Indexed: 11/06/2022]
Abstract
SCOPE To examine the association between milk and dairy products intake and the prevalence of cognitive decline among Spanish individuals at high cardiovascular risk. METHODS AND RESULTS Cross-sectional analyses are performed on baseline data from 6744 adults (aged 55-75 years old). Intake of milk and dairy products is estimated using a food frequency questionnaire grouped into quartiles. The risk of developing cognitive impairment is based on the Mini-Mental State Examination (MMSE). A higher prevalence of cognitive decline was found in subjects who consumed more grams. Patients with worse MMSE score (10-24) consumed a mean of 395.14 ± 12.21 g, while patients with better MMSE score (27-30) consumed a mean of 341.23 ± 2.73 g (p < 0.05). Those subjects with the lower milk consumption (<220 g/day) had a higher MMSE score (28.35 ± 0.045). Higher intake of fermented dairy products was observed in participants with a lower MMSE score (OR 1.340, p = 0.003). A positive correlation was found between the consumption of whole milk and the MMSE score (r = 0.066, p < 0.001). CONCLUSIONS These findings suggest that greater consumption of milk and dairy products could be associated with greater cognitive decline according to MMSE. Conversely, consumption of whole-fat milk could be linked with less cognitive impairment in the cross-sectional study.
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Affiliation(s)
- Araceli Muñoz-Garach
- Department of Endocrinology and Nutrition, Virgen de la Victoria University Hospital, Malaga University. Instituto de Investigación Biomédica de Málaga (IBIMA), Avda. Teatinos s/n., Málaga, 29010, Spain
| | - Isabel Cornejo-Pareja
- Department of Endocrinology and Nutrition, Virgen de la Victoria University Hospital, Malaga University. Instituto de Investigación Biomédica de Málaga (IBIMA), Avda. Teatinos s/n., Málaga, 29010, Spain
- Centro de Investigación Biomédica en Red Fisiopatología de la Obesidad y la Nutrición (CIBEROBN), Institute of Health Carlos III, C/ Monforte de Lemos, 5., Madrid, 28029, Spain
| | - Miguel Ángel Martínez-González
- Centro de Investigación Biomédica en Red Fisiopatología de la Obesidad y la Nutrición (CIBEROBN), Institute of Health Carlos III, C/ Monforte de Lemos, 5., Madrid, 28029, Spain
- Department of Preventive Medicine and Public Health, University of Navarra, IDISNA. C/ Irunlarrea, 1, Pamplona, Navarra, 31008, Spain
- Department of Nutrition, Harvard T.H. Chan School of Public Health. 665 Huntington Avenue Boston, Massachusetts, 02115, USA
| | - Monica Bulló
- Centro de Investigación Biomédica en Red Fisiopatología de la Obesidad y la Nutrición (CIBEROBN), Institute of Health Carlos III, C/ Monforte de Lemos, 5., Madrid, 28029, Spain
- Departament de Bioquímica i Biotecnologia, Unitat de Nutrició. Universitat Rovira i Virgili, Campus Sescelades. C/ Marcel·lí Domingo, 1., Reus, Tarragona, 43007, Spain
- Nutrition Unit. University Hospital of Sant Joan de Reus., Avinguda del Doctor Josep Laporte, 2, Reus, Tarragona, 43204, Spain
- Institut d'Investigació Sanitària Pere Virgili (IISPV)., Carrer Dr. Mallafré Guasch, 4., Reus, Tarragona, 43007, Spain
| | - Dolores Corella
- Centro de Investigación Biomédica en Red Fisiopatología de la Obesidad y la Nutrición (CIBEROBN), Institute of Health Carlos III, C/ Monforte de Lemos, 5., Madrid, 28029, Spain
- Department of Preventive Medicine, University of Valencia., Av. de Blasco Ibáñez, 13., Valencia, 46010, Spain
| | - Olga Castañer
- Unit of Cardiovascular Risk and Nutrition, Institut Hospital del Mar de Investigaciones Médicas Municipal d`Investigació Médica (IMIM)., Carrer del Dr. Aiguader, 88., Barcelona, 08003, Spain
| | - Dora Romaguera
- Centro de Investigación Biomédica en Red Fisiopatología de la Obesidad y la Nutrición (CIBEROBN), Institute of Health Carlos III, C/ Monforte de Lemos, 5., Madrid, 28029, Spain
- Health Research Institute of the Balearic Islands (IdISBa). Edificio S, Hospital Universitario Son Espases, Carretera de Valldemossa, 79., Palma, Balearic Islands, 07120, Spain
| | - Jesús Vioque
- CIBER de Epidemiología y Salud Pública (CIBERESP), Instituto de Salud Carlos III, C/ Monforte de Lemos, 5., Madrid, 28029, Spain
- Miguel Hernandez University, ISABIAL-FISABIO, Avda Pintor Baeza, 12 HGUA. Centro de Diagnóstico., Planta 5ª., Alicante, 03010, Spain
| | - Ángel M Alonso-Gómez
- Centro de Investigación Biomédica en Red Fisiopatología de la Obesidad y la Nutrición (CIBEROBN), Institute of Health Carlos III, C/ Monforte de Lemos, 5., Madrid, 28029, Spain
- Department of Cardiology, Organización Sanitaria Integrada (OSI) ARABA, University Hospital Araba, C/ Jose Atxotegi Kalea, s/n., Araba Vitoria-Gasteiz, 01009, Spain
- University of the Basque Country UPV/EHU, C/ Nieves Cano Kalea, 12., Araba Vitoria-Gasteiz, 01006, Spain
| | - Julia Wärnberg
- Centro de Investigación Biomédica en Red Fisiopatología de la Obesidad y la Nutrición (CIBEROBN), Institute of Health Carlos III, C/ Monforte de Lemos, 5., Madrid, 28029, Spain
- Department of Nursing, School of Health Sciences, University of Málaga-Institute of Biomedical Research in Malaga (IBIMA), Calle Severo Ochoa, 63., Málaga, 29590, Spain
| | - J Alfredo Martínez
- Centro de Investigación Biomédica en Red Fisiopatología de la Obesidad y la Nutrición (CIBEROBN), Institute of Health Carlos III, C/ Monforte de Lemos, 5., Madrid, 28029, Spain
- Department of Nutrition, Food Sciences, and Physiology, Center for Nutrition Research, University of Navarra, C/ Irunlarrea 1., Pamplona, Navarra, 31008, Spain
- Nutritional Genomics and Epigenomics Group, IMDEA Food, CEI UAM + CSIC, Crta. de, Carr. de Canto Blanco, 8., Madrid, 28049, Spain
| | - Luís Serra-Majem
- Centro de Investigación Biomédica en Red Fisiopatología de la Obesidad y la Nutrición (CIBEROBN), Institute of Health Carlos III, C/ Monforte de Lemos, 5., Madrid, 28029, Spain
- Nutrition Research Group, Research Institute of Biomedical and Health Sciences (IUIBS), University of Las Palmas de Gran Canaria, Instituto Universitario de Investigaciones Biomédicas y Sanitarias (iUIBS)., Paseo Blas Cabrera Felipe "Físico" (s/n)., 35016 - Las Palmas de Gran Canaria Islas Canarias, Spain
| | - Ramon Estruch
- Centro de Investigación Biomédica en Red Fisiopatología de la Obesidad y la Nutrición (CIBEROBN), Institute of Health Carlos III, C/ Monforte de Lemos, 5., Madrid, 28029, Spain
- Department of Internal Medicine, Institut d'Investigacions Biomèdiques August Pi Sunyer (IDIBAPS), Hospital Clinic, University of Barcelona, Carrer del Rosselló, 149., Barcelona, 08036, Spain
| | - M Rosa Bernal-López
- Centro de Investigación Biomédica en Red Fisiopatología de la Obesidad y la Nutrición (CIBEROBN), Institute of Health Carlos III, C/ Monforte de Lemos, 5., Madrid, 28029, Spain
- Department of Internal Medicine, Regional University Hospital of Malaga, Instituto de Investigación Biomédica de Malaga (IBIMA), Plaza del Hospital Civil, s/n., Malaga, 29009, Spain
| | - José Lapetra
- Centro de Investigación Biomédica en Red Fisiopatología de la Obesidad y la Nutrición (CIBEROBN), Institute of Health Carlos III, C/ Monforte de Lemos, 5., Madrid, 28029, Spain
- Department of Family Medicine, Research Unit, Distrito Sanitario Atención Primaria Sevilla, Edificio Isla, Av. de Ramón y Cajal, 9., Sevilla, 41005, Spain
| | - Xavier Pintó
- Centro de Investigación Biomédica en Red Fisiopatología de la Obesidad y la Nutrición (CIBEROBN), Institute of Health Carlos III, C/ Monforte de Lemos, 5., Madrid, 28029, Spain
- Lipids and Vascular Risk Unit, Internal Medicine, Hospital Universitario de Bellvitge-IDIBELL, Hospitalet de Llobregat., Universidad de Barcelona, Carrer de la Feixa Llarga, s/n., 08907 L'Hospitalet de Llobregat, Barcelona, Spain
- Medicine Department. Universidad de Barcelona, Calle Gran Via de les Corts Catalanes, 585., Barcelona, 08007, Spain
| | - Josep A Tur
- Centro de Investigación Biomédica en Red Fisiopatología de la Obesidad y la Nutrición (CIBEROBN), Institute of Health Carlos III, C/ Monforte de Lemos, 5., Madrid, 28029, Spain
- Research Group on Community Nutrition & Oxidative Stress, University of Balearic Islands, Carretera de Valldemossa, km 7.5., Palma de Mallorca, 07122, Spain
| | - José López-Miranda
- Centro de Investigación Biomédica en Red Fisiopatología de la Obesidad y la Nutrición (CIBEROBN), Institute of Health Carlos III, C/ Monforte de Lemos, 5., Madrid, 28029, Spain
- Department of Internal Medicine, Maimonides Biomedical Research Institute of Cordoba (IMIBIC), Reina Sofia University Hospital, University of Cordoba, Av. Menendez Pidal, s/n., Cordoba, 14004, Spain
| | - Aurora Bueno-Cavanillas
- CIBER de Epidemiología y Salud Pública (CIBERESP), Instituto de Salud Carlos III, C/ Monforte de Lemos, 5., Madrid, 28029, Spain
- Department of Preventive Medicine and Public Health, University of Granada, Av. del Hospicio, 1., Granada, 18010, Spain
| | - Miguel Delgado-Rodríguez
- CIBER de Epidemiología y Salud Pública (CIBERESP), Instituto de Salud Carlos III, C/ Monforte de Lemos, 5., Madrid, 28029, Spain
- Division of Preventive Medicine, Faculty of Medicine, University of Jaén, Campus Las Lagunillas, s/n., Jaén, 23071, Spain
| | - Pilar Matía-Martín
- Department of Endocrinology and Nutrition, Instituto de Investigación Sanitaria Hospital Clínico San Carlos (IdISSC), Calle del Prof Martín Lagos, s/n., Madrid, 28040, Spain
| | - Lidia Daimiel
- Nutritional Genomics and Epigenomics Group, IMDEA Food, CEI UAM + CSIC, Crta. de, Carr. de Canto Blanco, 8., Madrid, 28049, Spain
| | - Vicente Martín Sánchez
- CIBER de Epidemiología y Salud Pública (CIBERESP), Instituto de Salud Carlos III, C/ Monforte de Lemos, 5., Madrid, 28029, Spain
- Institute of Biomedicine (IBIOMED), University of León, Campus Universitario de Vegazana s/n., León, 24071, Spain
| | - Josep Vidal
- CIBER Diabetes y Enfermedades Metabólicas (CIBERDEM), Instituto de Salud Carlos III (ISCIII), C/ Monforte de Lemos, 5., Madrid, 28029, Spain
- Department of Endocrinology, Institut d` Investigacions Biomédiques August Pi Sunyer (IDIBAPS), Hospital Clinic, University of Barcelona, Carrer del Rosselló, 149., Barcelona, 08036, Spain
| | - Lucia Prieto
- Department of Endocrinology, Fundación Jiménez-Díaz, Av. de los Reyes Católicos, 2., Madrid, 28040, Spain
| | - Emilio Ros
- Centro de Investigación Biomédica en Red Fisiopatología de la Obesidad y la Nutrición (CIBEROBN), Institute of Health Carlos III, C/ Monforte de Lemos, 5., Madrid, 28029, Spain
- Lipid Clinic, Department of Endocrinology and Nutrition, Institut d'Investigacions Biomèdiques August Pi Sunyer (IDIBAPS), Hospital Clínic, Carrer del Rosselló, 149., Barcelona, 08036, Spain
| | - Fernando Fernández-Aranda
- Centro de Investigación Biomédica en Red Fisiopatología de la Obesidad y la Nutrición (CIBEROBN), Institute of Health Carlos III, C/ Monforte de Lemos, 5., Madrid, 28029, Spain
- Department of Psychiatry, University Hospital of Bellvitge-IDIBELL and Department of Clinical Sciences, School of Medicine and Health Sciences., University of Barcelona, Campus de Bellvitge, Feixa Llarga, s/n., 08907 L'Hospitalet de Llobregat Barcelona, Spain
| | - Lucía Camacho-Barcia
- Centro de Investigación Biomédica en Red Fisiopatología de la Obesidad y la Nutrición (CIBEROBN), Institute of Health Carlos III, C/ Monforte de Lemos, 5., Madrid, 28029, Spain
- Departament de Bioquímica i Biotecnologia, Unitat de Nutrició. Universitat Rovira i Virgili, Campus Sescelades. C/ Marcel·lí Domingo, 1., Reus, Tarragona, 43007, Spain
- Nutrition Unit. University Hospital of Sant Joan de Reus., Avinguda del Doctor Josep Laporte, 2, Reus, Tarragona, 43204, Spain
- Institut d'Investigació Sanitària Pere Virgili (IISPV)., Carrer Dr. Mallafré Guasch, 4., Reus, Tarragona, 43007, Spain
| | - Carolina Ortega-Azorin
- Centro de Investigación Biomédica en Red Fisiopatología de la Obesidad y la Nutrición (CIBEROBN), Institute of Health Carlos III, C/ Monforte de Lemos, 5., Madrid, 28029, Spain
- Department of Preventive Medicine, University of Valencia., Av. de Blasco Ibáñez, 13., Valencia, 46010, Spain
| | - María Soria
- Unit of Cardiovascular Risk and Nutrition, Institut Hospital del Mar de Investigaciones Médicas Municipal d`Investigació Médica (IMIM)., Carrer del Dr. Aiguader, 88., Barcelona, 08003, Spain
| | - Miquel Fiol
- Centro de Investigación Biomédica en Red Fisiopatología de la Obesidad y la Nutrición (CIBEROBN), Institute of Health Carlos III, C/ Monforte de Lemos, 5., Madrid, 28029, Spain
- Health Research Institute of the Balearic Islands (IdISBa). Edificio S, Hospital Universitario Son Espases, Carretera de Valldemossa, 79., Palma, Balearic Islands, 07120, Spain
| | - Laura Compañ-Gabucio
- CIBER de Epidemiología y Salud Pública (CIBERESP), Instituto de Salud Carlos III, C/ Monforte de Lemos, 5., Madrid, 28029, Spain
- Miguel Hernandez University, ISABIAL-FISABIO, Avda Pintor Baeza, 12 HGUA. Centro de Diagnóstico., Planta 5ª., Alicante, 03010, Spain
| | - Leire Goicolea-Güemez
- Department of Cardiology, Organización Sanitaria Integrada (OSI) ARABA, University Hospital Araba, C/ Jose Atxotegi Kalea, s/n., Araba Vitoria-Gasteiz, 01009, Spain
| | - Jessica Pérez-López
- Centro de Investigación Biomédica en Red Fisiopatología de la Obesidad y la Nutrición (CIBEROBN), Institute of Health Carlos III, C/ Monforte de Lemos, 5., Madrid, 28029, Spain
- Department of Nursing, School of Health Sciences, University of Málaga-Institute of Biomedical Research in Malaga (IBIMA), Calle Severo Ochoa, 63., Málaga, 29590, Spain
| | - Nuria Goñi
- Navarro Health Service., Primary Care Pamplona, Plaza de la Paz s/n., Navarra, 31002, Spain
| | - Judith Pérez-Cabrera
- Centro de Investigación Biomédica en Red Fisiopatología de la Obesidad y la Nutrición (CIBEROBN), Institute of Health Carlos III, C/ Monforte de Lemos, 5., Madrid, 28029, Spain
- Nutrition Research Group, Research Institute of Biomedical and Health Sciences (IUIBS), University of Las Palmas de Gran Canaria, Instituto Universitario de Investigaciones Biomédicas y Sanitarias (iUIBS)., Paseo Blas Cabrera Felipe "Físico" (s/n)., 35016 - Las Palmas de Gran Canaria Islas Canarias, Spain
| | - E Sacanella
- Centro de Investigación Biomédica en Red Fisiopatología de la Obesidad y la Nutrición (CIBEROBN), Institute of Health Carlos III, C/ Monforte de Lemos, 5., Madrid, 28029, Spain
- Department of Internal Medicine, Institut d'Investigacions Biomèdiques August Pi Sunyer (IDIBAPS), Hospital Clinic, University of Barcelona, Carrer del Rosselló, 149., Barcelona, 08036, Spain
| | - Jose Carlos Fernández-García
- Department of Endocrinology and Nutrition, Virgen de la Victoria University Hospital, Malaga University. Instituto de Investigación Biomédica de Málaga (IBIMA), Avda. Teatinos s/n., Málaga, 29010, Spain
- Centro de Investigación Biomédica en Red Fisiopatología de la Obesidad y la Nutrición (CIBEROBN), Institute of Health Carlos III, C/ Monforte de Lemos, 5., Madrid, 28029, Spain
| | - Leticia Miró-Moriano
- Centro de Investigación Biomédica en Red Fisiopatología de la Obesidad y la Nutrición (CIBEROBN), Institute of Health Carlos III, C/ Monforte de Lemos, 5., Madrid, 28029, Spain
- Department of Family Medicine, Research Unit, Distrito Sanitario Atención Primaria Sevilla, Edificio Isla, Av. de Ramón y Cajal, 9., Sevilla, 41005, Spain
| | - M Gimenez-Gracia
- Centro de Investigación Biomédica en Red Fisiopatología de la Obesidad y la Nutrición (CIBEROBN), Institute of Health Carlos III, C/ Monforte de Lemos, 5., Madrid, 28029, Spain
- Department of Family Medicine, Research Unit, Distrito Sanitario Atención Primaria Sevilla, Edificio Isla, Av. de Ramón y Cajal, 9., Sevilla, 41005, Spain
| | - C Razquin
- Centro de Investigación Biomédica en Red Fisiopatología de la Obesidad y la Nutrición (CIBEROBN), Institute of Health Carlos III, C/ Monforte de Lemos, 5., Madrid, 28029, Spain
- Department of Preventive Medicine and Public Health, University of Navarra, IDISNA. C/ Irunlarrea, 1, Pamplona, Navarra, 31008, Spain
- Department of Nutrition, Harvard T.H. Chan School of Public Health. 665 Huntington Avenue Boston, Massachusetts, 02115, USA
| | - Indira Paz-Graniel
- Departament de Bioquímica i Biotecnologia, Unitat de Nutrició. Universitat Rovira i Virgili, Campus Sescelades. C/ Marcel·lí Domingo, 1., Reus, Tarragona, 43007, Spain
- Nutrition Unit. University Hospital of Sant Joan de Reus., Avinguda del Doctor Josep Laporte, 2, Reus, Tarragona, 43204, Spain
| | - Patricia Guillem
- Centro de Investigación Biomédica en Red Fisiopatología de la Obesidad y la Nutrición (CIBEROBN), Institute of Health Carlos III, C/ Monforte de Lemos, 5., Madrid, 28029, Spain
- Department of Preventive Medicine, University of Valencia., Av. de Blasco Ibáñez, 13., Valencia, 46010, Spain
| | - María Dolors Zomeño
- Unit of Cardiovascular Risk and Nutrition, Institut Hospital del Mar de Investigaciones Médicas Municipal d`Investigació Médica (IMIM)., Carrer del Dr. Aiguader, 88., Barcelona, 08003, Spain
| | - Manuel Moñino
- Centro de Investigación Biomédica en Red Fisiopatología de la Obesidad y la Nutrición (CIBEROBN), Institute of Health Carlos III, C/ Monforte de Lemos, 5., Madrid, 28029, Spain
- Health Research Institute of the Balearic Islands (IdISBa). Edificio S, Hospital Universitario Son Espases, Carretera de Valldemossa, 79., Palma, Balearic Islands, 07120, Spain
| | - Alejandro Oncina-Canovas
- CIBER de Epidemiología y Salud Pública (CIBERESP), Instituto de Salud Carlos III, C/ Monforte de Lemos, 5., Madrid, 28029, Spain
- Miguel Hernandez University, ISABIAL-FISABIO, Avda Pintor Baeza, 12 HGUA. Centro de Diagnóstico., Planta 5ª., Alicante, 03010, Spain
| | - Itziar Salaverria-Lete
- Department of Cardiology, Organización Sanitaria Integrada (OSI) ARABA, University Hospital Araba, C/ Jose Atxotegi Kalea, s/n., Araba Vitoria-Gasteiz, 01009, Spain
| | - Estefanía Toledo
- Centro de Investigación Biomédica en Red Fisiopatología de la Obesidad y la Nutrición (CIBEROBN), Institute of Health Carlos III, C/ Monforte de Lemos, 5., Madrid, 28029, Spain
- Department of Preventive Medicine and Public Health, University of Navarra, IDISNA. C/ Irunlarrea, 1, Pamplona, Navarra, 31008, Spain
- Department of Nutrition, Harvard T.H. Chan School of Public Health. 665 Huntington Avenue Boston, Massachusetts, 02115, USA
| | - Jordi Salas-Salvadó
- Centro de Investigación Biomédica en Red Fisiopatología de la Obesidad y la Nutrición (CIBEROBN), Institute of Health Carlos III, C/ Monforte de Lemos, 5., Madrid, 28029, Spain
- Departament de Bioquímica i Biotecnologia, Unitat de Nutrició. Universitat Rovira i Virgili, Campus Sescelades. C/ Marcel·lí Domingo, 1., Reus, Tarragona, 43007, Spain
- Nutrition Unit. University Hospital of Sant Joan de Reus., Avinguda del Doctor Josep Laporte, 2, Reus, Tarragona, 43204, Spain
- Institut d'Investigació Sanitària Pere Virgili (IISPV)., Carrer Dr. Mallafré Guasch, 4., Reus, Tarragona, 43007, Spain
| | - Helmut Schröder
- Unit of Cardiovascular Risk and Nutrition, Institut Hospital del Mar de Investigaciones Médicas Municipal d`Investigació Médica (IMIM)., Carrer del Dr. Aiguader, 88., Barcelona, 08003, Spain
- CIBER de Epidemiología y Salud Pública (CIBERESP), Instituto de Salud Carlos III, C/ Monforte de Lemos, 5., Madrid, 28029, Spain
| | - Francisco J Tinahones
- Department of Endocrinology and Nutrition, Virgen de la Victoria University Hospital, Malaga University. Instituto de Investigación Biomédica de Málaga (IBIMA), Avda. Teatinos s/n., Málaga, 29010, Spain
- Centro de Investigación Biomédica en Red Fisiopatología de la Obesidad y la Nutrición (CIBEROBN), Institute of Health Carlos III, C/ Monforte de Lemos, 5., Madrid, 28029, Spain
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Abstract
Alzheimer's disease (AD) research, treatment, and prevention focus increasingly on developing personalized interventions based on personal genetic, biological, phenotypic data, for early intervention (EI) to limit harm. This approach has much to recommend it, but important ethical and philosophical challenges follow that should be considered, which we analyze here. We argue that advancing understanding of the causes of AD undermines the clarity of the distinction between primary and secondary prevention. This makes it increasingly unclear how primary and secondary categories can be appealed to as the basis for making judgements about what interventions are permissible, and for distinguishing between acceptably vs unacceptably early points in life to intervene. Timely efforts at prevention are vital for limiting harm from AD and given the logic of EI is that, in presence of risk, earlier is better, one might assume that earliest is best. This may or may not be the case; however, the permissibility of intervening in different ways at different stages of life is complex and turns on numerous contextual factors. We consider the particular ethical implications of intervening at different points in the life course, presenting a valuable resource for negotiating clinical and policy implications of EI in AD.
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Affiliation(s)
- Alex McKeown
- University of Oxford and Wellcome Centre for Ethics and Humanities
| | - Gin S Malhi
- University of Sydney Faculty of Medicine and Health
| | - Ilina Singh
- University of Oxford and Wellcome Centre for Ethics and Humanities
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Abstract
A three-part mechanism is proposed for the induction of Alzheimer’s disease: (1) decreased blood lactic acid; (2) increased blood ceramide and adipokines; (3) decreased blood folic acid. The age-related nature of these mechanisms comes from age-associated decreased muscle mass, increased visceral fat and changes in diet. This mechanism also explains why many people do not develop Alzheimer’s disease. Simple changes in lifestyle and diet can prevent Alzheimer’s disease. Alzheimer’s disease is caused by a cascade of events that culminates in damage to the blood–brain barrier and damage to neurons. The blood–brain barrier keeps toxic molecules out of the brain and retains essential molecules in the brain. Lactic acid is a nutrient to the brain and is produced by exercise. Damage to endothelial cells and pericytes by inadequate lactic acid leads to blood–brain barrier damage and brain damage. Inadequate folate intake and oxidative stress induced by activation of transient receptor potential cation channels and endothelial nitric oxide synthase damage the blood–brain barrier. NAD depletion due to inadequate intake of nicotinamide and alterations in the kynurenine pathway damages neurons. Changes in microRNA levels may be the terminal events that cause neuronal death leading to Alzheimer’s disease. A new mechanism of Alzheimer’s disease induction is presented involving lactic acid, ceramide, IL-1β, tumor necrosis factor α, folate, nicotinamide, kynurenine metabolites and microRNA.
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Wesselman LMP, van Lent DM, Schröder A, van de Rest O, Peters O, Menne F, Fuentes M, Priller J, Spruth EJ, Altenstein S, Schneider A, Fließbach K, Roeske S, Wolfsgruber S, Kleineidam L, Spottke A, Pross V, Wiltfang J, Vukovich R, Schild AK, Düzel E, Metzger CD, Glanz W, Buerger K, Janowitz D, Perneczky R, Tatò M, Teipel S, Kilimann I, Laske C, Buchmann M, Ramirez A, Sikkes SAM, Jessen F, van der Flier WM, Wagner M. Dietary patterns are related to cognitive functioning in elderly enriched with individuals at increased risk for Alzheimer's disease. Eur J Nutr 2021; 60:849-860. [PMID: 32472387 PMCID: PMC7900077 DOI: 10.1007/s00394-020-02257-6] [Citation(s) in RCA: 29] [Impact Index Per Article: 7.3] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/08/2019] [Accepted: 04/22/2020] [Indexed: 12/15/2022]
Abstract
PURPOSE To investigate cross-sectional associations between dietary patterns and cognitive functioning in elderly free of dementia. METHODS Data of 389 participants from the German DELCODE study (52% female, 69 ± 6 years, mean Mini Mental State Score 29 ± 1) were included. The sample was enriched with elderly at increased risk for Alzheimer's disease (AD) by including participants with subjective cognitive decline, mild cognitive impairment (MCI) and siblings of AD patients. Mediterranean and MIND diets were derived from 148 Food Frequency Questionnaire items, and data-driven patterns by principal component analysis (PCA) of 39 food groups. Associations between dietary patterns and five cognitive domain scores were analyzed with linear regression analyses adjusted for demographics (model 1), and additionally for energy intake, BMI, other lifestyle variables and APOe4-status (model 2). For PCA-derived dietary components, final model 3 included all other dietary components. RESULTS In fully adjusted models, adherence to Mediterranean and MIND diet was associated with better memory. The 'alcoholic beverages' PCA component was positively associated with most cognitive domains. Exclusion of MCI subjects (n = 60) revealed that Mediterranean and MIND diet were also related to language functions; associations with the alcoholic beverages component were attenuated, but most remained significant. CONCLUSION In line with data from elderly population samples, Mediterranean and MIND diet and some data-derived dietary patterns were related to memory and language function. Longitudinal data are needed to draw conclusions on the putative effect of nutrition on the rate of cognitive decline, and on the potential of dietary interventions in groups at increased risk for AD.
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Affiliation(s)
- L. M. P. Wesselman
- German Center for Neurodegenerative Disorders (DZNE), Bonn, Venusberg-Campus 1, 53127 Bonn, Germany
- Department of Neurology, Alzheimer Center Amsterdam, Amsterdam Neuroscience, Vrije Universiteit Amsterdam, Amsterdam UMC, Amsterdam, The Netherlands
| | - D. Melo van Lent
- German Center for Neurodegenerative Disorders (DZNE), Bonn, Venusberg-Campus 1, 53127 Bonn, Germany
- The Glenn Biggs Institute for Alzheimer’s and Neurodegenerative Diseases, UT Health, San Antonio, TX USA
- Department of Neurology, Boston University, Boston, MA USA
- The Framingham Heart Study, Framingham, MA USA
| | - A. Schröder
- German Center for Neurodegenerative Disorders (DZNE), Bonn, Venusberg-Campus 1, 53127 Bonn, Germany
| | - O. van de Rest
- Division of Human Nutrition and Health, Wageningen University and Research, Wageningen, The Netherlands
| | - O. Peters
- German Center for Neurodegenerative Diseases (DZNE), Berlin, Germany
- Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Institute of Psychiatry and Psychotherapy, Hindenburgdamm 30, 12203 Berlin, Germany
| | - F. Menne
- Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Institute of Psychiatry and Psychotherapy, Hindenburgdamm 30, 12203 Berlin, Germany
| | - M. Fuentes
- Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Institute of Psychiatry and Psychotherapy, Hindenburgdamm 30, 12203 Berlin, Germany
| | - J. Priller
- German Center for Neurodegenerative Diseases (DZNE), Berlin, Germany
- Department of Psychiatry and Psychotherapy, Charité, Charitéplatz 1, 10117 Berlin, Germany
| | - E. J. Spruth
- German Center for Neurodegenerative Diseases (DZNE), Berlin, Germany
- Department of Psychiatry and Psychotherapy, Charité, Charitéplatz 1, 10117 Berlin, Germany
| | - S. Altenstein
- Department of Psychiatry and Psychotherapy, Charité, Charitéplatz 1, 10117 Berlin, Germany
| | - A. Schneider
- German Center for Neurodegenerative Disorders (DZNE), Bonn, Venusberg-Campus 1, 53127 Bonn, Germany
- Department for Neurodegenerative Diseases and Geriatric Psychiatry, University Hospital Bonn, Venusberg-Campus 1, 53127 Bonn, Germany
| | - K. Fließbach
- German Center for Neurodegenerative Disorders (DZNE), Bonn, Venusberg-Campus 1, 53127 Bonn, Germany
- Department for Neurodegenerative Diseases and Geriatric Psychiatry, University Hospital Bonn, Venusberg-Campus 1, 53127 Bonn, Germany
| | - S. Roeske
- German Center for Neurodegenerative Disorders (DZNE), Bonn, Venusberg-Campus 1, 53127 Bonn, Germany
| | - S. Wolfsgruber
- German Center for Neurodegenerative Disorders (DZNE), Bonn, Venusberg-Campus 1, 53127 Bonn, Germany
- Department for Neurodegenerative Diseases and Geriatric Psychiatry, University Hospital Bonn, Venusberg-Campus 1, 53127 Bonn, Germany
| | - L. Kleineidam
- German Center for Neurodegenerative Disorders (DZNE), Bonn, Venusberg-Campus 1, 53127 Bonn, Germany
- Department for Neurodegenerative Diseases and Geriatric Psychiatry, University Hospital Bonn, Venusberg-Campus 1, 53127 Bonn, Germany
| | - A. Spottke
- German Center for Neurodegenerative Disorders (DZNE), Bonn, Venusberg-Campus 1, 53127 Bonn, Germany
- Department of Neurology, University of Bonn, Venusberg-Campus 1, 53127 Bonn, Germany
| | - V. Pross
- Study Center Bonn, Medical Faculty, Venusberg-Campus 1, 53127 Bonn, Germany
| | - J. Wiltfang
- German Center for Neurodegenerative Diseases (DZNE), Goettingen, Germany
- Department of Psychiatry and Psychotherapy, University Medical Center Goettingen, University of Goettingen, Von-Siebold-Str. 5, 37075 Goettingen , Germany
| | - R. Vukovich
- German Center for Neurodegenerative Diseases (DZNE), Goettingen, Germany
- Department of Psychiatry and Psychotherapy, University Medical Center Goettingen, University of Goettingen, Von-Siebold-Str. 5, 37075 Goettingen , Germany
| | - A. K. Schild
- German Center for Neurodegenerative Disorders (DZNE), Bonn, Venusberg-Campus 1, 53127 Bonn, Germany
- Department of Psychiatry, University of Cologne, Medical Faculty, Kerpener Strasse 62, 50924 Cologne, Germany
| | - E. Düzel
- German Center for Neurodegenerative Diseases (DZNE), Magdeburg, Germany
- Institute of Cognitive Neurology and Dementia Research (IKND), Otto-Von-Guericke University, Magdeburg, Germany
| | - C. D. Metzger
- German Center for Neurodegenerative Diseases (DZNE), Magdeburg, Germany
- Institute of Cognitive Neurology and Dementia Research (IKND), Otto-Von-Guericke University, Magdeburg, Germany
- Department of Psychiatry and Psychotherapy, Otto-Von-Guericke University, Magdeburg, Germany
| | - W. Glanz
- German Center for Neurodegenerative Diseases (DZNE), Magdeburg, Germany
| | - K. Buerger
- German Center for Neurodegenerative Diseases (DZNE, Munich), Feodor-Lynen-Strasse 17, 81377 Munich, Germany
- Institute for Stroke and Dementia Research (ISD), University Hospital, LMU Munich, Feodor-Lynen-Strasse 17, 81377 Munich, Germany
| | - D. Janowitz
- Institute for Stroke and Dementia Research (ISD), University Hospital, LMU Munich, Feodor-Lynen-Strasse 17, 81377 Munich, Germany
| | - R. Perneczky
- German Center for Neurodegenerative Diseases (DZNE, Munich), Feodor-Lynen-Strasse 17, 81377 Munich, Germany
- Department of Psychiatry and Psychotherapy, University Hospital, LMU Munich, Munich, Germany
- Munich Cluster for Systems Neurology (SyNergy) Munich, Munich, Germany
- Ageing Epidemiology Research Unit (AGE), School of Public Health, Imperial College London, London, UK
| | - M. Tatò
- German Center for Neurodegenerative Diseases (DZNE, Munich), Feodor-Lynen-Strasse 17, 81377 Munich, Germany
| | - S. Teipel
- German Center for Neurodegenerative Diseases (DZNE), Rostock, Germany
- Department of Psychosomatic Medicine, Rostock University Medical Center, Gehlsheimer Str. 20, 18147 Rostock, Germany
| | - I. Kilimann
- German Center for Neurodegenerative Diseases (DZNE), Rostock, Germany
- Department of Psychosomatic Medicine, Rostock University Medical Center, Gehlsheimer Str. 20, 18147 Rostock, Germany
| | - C. Laske
- German Center for Neurodegenerative Diseases (DZNE), Tübingen, Germany
- Section for Dementia Research, Hertie Institute for Clinical Brain Research and Department of Psychiatry and Psychotherapy, University of Tübingen, Tübingen, Germany
| | - M. Buchmann
- German Center for Neurodegenerative Diseases (DZNE), Tübingen, Germany
- Section for Dementia Research, Hertie Institute for Clinical Brain Research and Department of Psychiatry and Psychotherapy, University of Tübingen, Tübingen, Germany
| | - A. Ramirez
- Department of Psychiatry, University of Cologne, Medical Faculty, Kerpener Strasse 62, 50924 Cologne, Germany
| | - S. A. M. Sikkes
- Department of Neurology, Alzheimer Center Amsterdam, Amsterdam Neuroscience, Vrije Universiteit Amsterdam, Amsterdam UMC, Amsterdam, The Netherlands
- Clinical Developmental Psychology and Clinical Neuropsychology, Faculty of Behavioural and Movement Sciences (FGB), Vrije University Amsterdam, Amsterdam, The Netherlands
| | - F. Jessen
- German Center for Neurodegenerative Disorders (DZNE), Bonn, Venusberg-Campus 1, 53127 Bonn, Germany
- Department of Psychiatry, University of Cologne, Medical Faculty, Kerpener Strasse 62, 50924 Cologne, Germany
| | - W. M. van der Flier
- Department of Neurology, Alzheimer Center Amsterdam, Amsterdam Neuroscience, Vrije Universiteit Amsterdam, Amsterdam UMC, Amsterdam, The Netherlands
- Department of Epidemiology and Biostatistics, Amsterdam Neuroscience, Vrije Universiteit Amsterdam, Amsterdam UMC, Amsterdam, The Netherlands
| | - M. Wagner
- German Center for Neurodegenerative Disorders (DZNE), Bonn, Venusberg-Campus 1, 53127 Bonn, Germany
- Department for Neurodegenerative Diseases and Geriatric Psychiatry, University Hospital Bonn, Venusberg-Campus 1, 53127 Bonn, Germany
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Gu Y, Guo J, Moshfegh AJ. Race/ethnicity and gender modify the association between diet and cognition in U.S. older adults: National Health and Nutrition Examination Survey 2011-2014. ALZHEIMER'S & DEMENTIA (NEW YORK, N. Y.) 2021; 7:e12128. [PMID: 33614896 PMCID: PMC7882526 DOI: 10.1002/trc2.12128] [Citation(s) in RCA: 10] [Impact Index Per Article: 2.5] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Download PDF] [Figures] [Subscribe] [Scholar Register] [Received: 08/03/2020] [Revised: 10/20/2020] [Accepted: 11/25/2020] [Indexed: 11/12/2022]
Abstract
INTRODUCTION It is unclear whether the association between Mediterranean-type Diet (MeDi) and cognition is similar across different racial/ethnic groups or between women and men. METHODS The current study included 2435 participants (≥60 years of age) of the National Health and Nutrition Examination Survey (NHANES) 2011-2014. Linear regression models were applied to examine the association between diet and cognition, adjusted for multiple demographic variables. Interaction between MeDi and race/ethnicity (non-Hispanic White, non-Hispanic Black, Hispanic, other), and between MeDi and gender, were examined, followed by stratified analyses. RESULTS One score increase in MeDi was associated with 0.039 (95%confidence interval [CI] = 0.016-0.062) higher global cognitive z-score. Significant associations between MeDi and global cognition and between MeDi and immediate recall were found in the non-Hispanic Whites only (P-interaction = 0.057 and 0.059, respectively). MeDi was associated with increased score of animal fluency score in men but not in women (P-interaction = 0.082). DISCUSSION The positive association between MeDi and cognition might be dependent on race/ethnicity and gender.
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Affiliation(s)
- Yian Gu
- Taub Institute for Research in Alzheimer's Disease and the Aging BrainColumbia UniversityNew YorkNew YorkUSA
- Department of NeurologyVagelos College of Physicians and SurgeonsColumbia UniversityNew YorkNew YorkUSA
- Gertrude H. Sergievsky CenterColumbia UniversityNew YorkNew YorkUSA
- Department of EpidemiologyJoseph P. Mailman School of Public HealthColumbia UniversityNew YorkNew YorkUSA
| | - Jing Guo
- Taub Institute for Research in Alzheimer's Disease and the Aging BrainColumbia UniversityNew YorkNew YorkUSA
| | - Alanna J Moshfegh
- Beltsville Human Nutrition Research CenterAgricultural Research ServiceUSDABeltsvilleMarylandUSA
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Fu J, Liu Q, Zhang M, Sun C, Du Y, Zhu Y, Lin H, Jin M, Ma F, Li W, Liu H, Yan J, Chen Y, Wang G, Huang G. Association between methionine cycle metabolite-related diets and mild cognitive impairment in older Chinese adults: a population-based observational study. Nutr Neurosci 2021; 25:1495-1508. [PMID: 33494658 DOI: 10.1080/1028415x.2021.1872959] [Citation(s) in RCA: 6] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 10/22/2022]
Abstract
BACKGROUND Homocysteine (Hcy) and folate, involved in a common metabolic pathway supplying essential methyl groups for DNA and protein synthesis, have been found to be associated with cognitive function. Moreover, diet may influence methionine cycle metabolites (MCM) as well as mild cognitive impairment (MCI), but MCM-related dietary patterns are unclear in an older population. OBJECTIVE The study aimed to identify MCM-related dietary patterns of older Chinese adults, and examine their association with the prevalence of MCI in a large population-based study. METHODS This study included 4457 participants ≥ 60 years of age from the Tianjin Elderly Nutrition and Cognition Cohort study. Dietary data were collected using a valid self-administered food frequency questionnaire, and factor analysis was used to identify major dietary patterns in the population. MCM-based dietary patterns were derived using reduced rank regression (RRR) based on serum folate and Hcy as response variables. RESULTS Compared with the participants in the lowest quartile of vegetarian pattern and processed foods pattern, the odds ratios (ORs) of MCI in the highest quartile were 0.72 (95% CI 0.53-0.98) and 1.39 (95% CI 1.03-1.88), respectively. In the MCM-based dietary patterns derived using RRR, the ORs for MCI for the highest quartile of MCM patterns I and II were 0.58 (95% CI 0.44-0.78) and 1.38 (95% CI 1.04-1.83), respectively, compared with participants in the lower quartile. CONCLUSIONS Findings from this large population-based study suggested that adopting an MCM-related dietary pattern, especially avoiding processed foods, can decrease the occurrence of MCI.
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Affiliation(s)
- Jingzhu Fu
- Department of Nutrition & Food Science, School of Public Health, Tianjin Medical University, Tianjin, People's Republic of China.,Tianjin Key Laboratory of Environment, Nutrition and Public Health, Tianjin, People's Republic of China
| | - Qian Liu
- Department of Nutrition & Food Science, School of Public Health, Tianjin Medical University, Tianjin, People's Republic of China.,Tianjin Key Laboratory of Environment, Nutrition and Public Health, Tianjin, People's Republic of China
| | - Meilin Zhang
- Department of Nutrition & Food Science, School of Public Health, Tianjin Medical University, Tianjin, People's Republic of China.,Tianjin Key Laboratory of Environment, Nutrition and Public Health, Tianjin, People's Republic of China
| | - Changqing Sun
- Neurosurgical Department of Baodi Clinical College of Tianjin Medical University, Tianjin, People's Republic of China
| | - Yue Du
- Tianjin Key Laboratory of Environment, Nutrition and Public Health, Tianjin, People's Republic of China.,Department of Social Medicine and Health Management, School of Public Health, Tianjin Medical University, Tianjin, People's Republic of China
| | - Yun Zhu
- Tianjin Key Laboratory of Environment, Nutrition and Public Health, Tianjin, People's Republic of China.,Department of Epidemiology & Biostatistics, School of Public Health, Tianjin Medical University, Tianjin, People's Republic of China
| | - Hongyan Lin
- Department of Nutrition & Food Science, School of Public Health, Tianjin Medical University, Tianjin, People's Republic of China.,Tianjin Key Laboratory of Environment, Nutrition and Public Health, Tianjin, People's Republic of China
| | - Mengdi Jin
- Department of Nutrition & Food Science, School of Public Health, Tianjin Medical University, Tianjin, People's Republic of China.,Tianjin Key Laboratory of Environment, Nutrition and Public Health, Tianjin, People's Republic of China
| | - Fei Ma
- Tianjin Key Laboratory of Environment, Nutrition and Public Health, Tianjin, People's Republic of China.,Department of Epidemiology & Biostatistics, School of Public Health, Tianjin Medical University, Tianjin, People's Republic of China
| | - Wen Li
- Department of Nutrition & Food Science, School of Public Health, Tianjin Medical University, Tianjin, People's Republic of China.,Tianjin Key Laboratory of Environment, Nutrition and Public Health, Tianjin, People's Republic of China
| | - Huan Liu
- Department of Nutrition & Food Science, School of Public Health, Tianjin Medical University, Tianjin, People's Republic of China.,Tianjin Key Laboratory of Environment, Nutrition and Public Health, Tianjin, People's Republic of China
| | - Jing Yan
- Tianjin Key Laboratory of Environment, Nutrition and Public Health, Tianjin, People's Republic of China.,Department of Social Medicine and Health Management, School of Public Health, Tianjin Medical University, Tianjin, People's Republic of China
| | - Yongjie Chen
- Tianjin Key Laboratory of Environment, Nutrition and Public Health, Tianjin, People's Republic of China.,Department of Epidemiology & Biostatistics, School of Public Health, Tianjin Medical University, Tianjin, People's Republic of China
| | - Guangshun Wang
- Department of Tumor, Baodi Clinical College of Tianjin Medical University, Tianjin, People's Republic of China
| | - Guowei Huang
- Department of Nutrition & Food Science, School of Public Health, Tianjin Medical University, Tianjin, People's Republic of China.,Tianjin Key Laboratory of Environment, Nutrition and Public Health, Tianjin, People's Republic of China
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Moradi S, Moloudi J, Moradinazar M, Sarokhani D, Nachvak SM, Samadi M. Adherence to Healthy Diet Can Delay Alzheimer's Diseases Development: A Systematic Review and Meta-Analysis. Prev Nutr Food Sci 2020; 25:325-337. [PMID: 33505926 PMCID: PMC7813603 DOI: 10.3746/pnf.2020.25.4.325] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/24/2020] [Accepted: 09/15/2020] [Indexed: 11/07/2022] Open
Abstract
A healthy diet has long been indicated to be protective against Alzheimer’s diseases (AD). We carried out a systematic review and meta-analysis of published observational studies to explore the relationship between healthy and unhealthy diets and risk of ADs. We screened PubMed, Scopus, Web of Sciences, Google Scholar, Science Direct, and Embase, and screened manually to identify relevant articles published in English and non-English until Jun 2020. We classified the studied dietary patterns into two groups: healthy and unhealthy diets. The pooled weighted mean difference and 95% confidence interval (95% CI) was used to analyze the data using a random-effects model. The data were extracted manually and the preferred reporting items for systematic review and meta-analysis checklist was used to appraise the risk of bias and quality of data. Of the 1,813 articles identified, 21 met the inclusion criteria and were included in the quantitative analysis. A healthy diet was related to a lower risk of AD [odds ratio (OR): 0.45, 95% CI: 0.23 to 0.86, I2=99.7%; n=17 studies]. Moreover, high adherence to an unhealthy diet was not associated with increased risk of AD (OR: 0.99, 95% CI: 0.98 to 0.99, I2=0.0%; n=6 studies). However, the etiology of AD is uncertain and it is difficult draw conclusions about dietary healthy patterns. We concluded that adherence to a healthy diet is associated with a lower risk of AD, but were unable to find evidence that an unhealthy diet increases the risk of AD.
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Affiliation(s)
- Shima Moradi
- Department of Nutritional Sciences, Research Center for Environmental Determinants of Health (RCEDH), Health Institute, Kermanshah 67198-51351, Iran
| | - Jalall Moloudi
- Department of Nutritional Sciences, Research Center for Environmental Determinants of Health (RCEDH), Health Institute, Kermanshah 67198-51351, Iran.,Student Research Committee, Kermanshah University of Medical Sciences, Kermanshah 67198-51351, Iran
| | - Mehdi Moradinazar
- Behavioral Disease Research Center, Kermanshah University of Medical Sciences, Kermanshah 67198-51351, Iran
| | - Diana Sarokhani
- Psychosocial Injuries Research Center, Ilam University of Medical Sciences, Ilam 69311-57793, Iran
| | - Seyyed Mostafa Nachvak
- Department of Nutritional Sciences, Research Center for Environmental Determinants of Health (RCEDH), Health Institute, Kermanshah 67198-51351, Iran
| | - Mehnoosh Samadi
- Department of Nutritional Sciences, Research Center for Environmental Determinants of Health (RCEDH), Health Institute, Kermanshah 67198-51351, Iran
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Frölich L. Alzheimer's disease - the 'microbial hypothesis' from a clinical and neuroimaging perspective. Psychiatry Res Neuroimaging 2020; 306:111181. [PMID: 32919870 DOI: 10.1016/j.pscychresns.2020.111181] [Citation(s) in RCA: 19] [Impact Index Per Article: 3.8] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 06/06/2020] [Revised: 06/25/2020] [Accepted: 09/03/2020] [Indexed: 12/18/2022]
Abstract
The etiology of Alzheimer's disease (AD) is under debate since its first description in 1906. Extracellular senile plaques composed of beta-amyloid peptide (Aβ) and intracellular neurofibrillary tangles composed of tau protein characterize the histopathology of the disease. The 'amyloid cascade hypothesis' summarizes the molecular mechanisms leading to deposition of these proteins. However, treatments derived from this hypothesis have been unsuccessful. An infectious etiology for AD has been repeatedly proposed. Neurotropic viruses, gut and lung bacteriae, and Bovine Meat and Milk Factors have been implicated in neurodegenerative disorders including AD. These pathogens may act directly or as a trigger or co-factor for inducing neurodegeneration in AD. The antimicrobial properties of beta-amyloid have shifted the discussion of the etiological origin of AD towards an interaction hypothesis. Neuroimaging studies have added to the understanding of mechanisms involved in neurodegeneration. Antiviral agents and a bacterial protease inhibitor targeting Porphyromonas gingivalis toxins are currently tested in clinical trials. Further clinical studies are needed to test if strategies directly derived from the 'microbial hypothesis' or combination strategies including antimicrobial agents may be beneficial for patients with Alzheimer's disease.
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Affiliation(s)
- Lutz Frölich
- Dept of Geriatric Psychiatry, Central Institute of Mental Health, Medical Faculty Mannheim, University of Heidelberg, Germany.
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Gruendler R, Hippe B, Sendula Jengic V, Peterlin B, Haslberger AG. Nutraceutical Approaches of Autophagy and Neuroinflammation in Alzheimer's Disease: A Systematic Review. Molecules 2020; 25:molecules25246018. [PMID: 33353228 PMCID: PMC7765980 DOI: 10.3390/molecules25246018] [Citation(s) in RCA: 18] [Impact Index Per Article: 3.6] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/01/2020] [Revised: 12/15/2020] [Accepted: 12/16/2020] [Indexed: 12/11/2022] Open
Abstract
Aging and the emergence of age-associated illnesses are one of the major challenges of our present society. Alzheimer’s disease (AD) is closely associated with aging and is defined by increasing memory loss and severe dementia. Currently, there are no therapy options available that halt AD progression. This work investigates three hallmarks of the disease (autophagy, neuroinflammation, and senescence) and systematically analyzes if there is a beneficial effect from three substances derived from food sources, the so called “nutraceuticals” epigallocatechin gallate, fisetin, and spermidine, on these hallmarks. The results imply a positive outlook for the reviewed substances to qualify as a novel treatment option for AD. A combination of nutraceutical substances and other preventive measures could have significant clinical impact in a multi-layered therapy approach to counter AD.
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Affiliation(s)
- Reinhard Gruendler
- Department of Pharmacology and Toxicology, University of Vienna, A-1090 Vienna, Austria;
| | - Berit Hippe
- Department of Nutritional Sciences, University of Vienna, A-1090 Vienna, Austria;
| | | | | | - Alexander G. Haslberger
- Department of Nutritional Sciences, University of Vienna, A-1090 Vienna, Austria;
- Correspondence:
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Bermejo-Pareja F, Ciudad-Cabañas MJ, Llamas-Velasco S, Tapias-Merino E, Hernández Gallego J, Hernández-Cabria M, Collado-Yurrita L, López-Arrieta JM. Is milk and dairy intake a preventive factor for elderly cognition (dementia and Alzheimer's)? A quality review of cohort surveys. Nutr Rev 2020; 79:743-757. [PMID: 33316068 DOI: 10.1093/nutrit/nuaa045] [Citation(s) in RCA: 9] [Impact Index Per Article: 1.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/14/2022] Open
Abstract
Milk and dairy (M&D) is a longstanding human food with widespread use. Many studies showed the preventive capacity of M&D in several human health disorders, but its utility in others is under discussion. Aging has been associated to elderly cognitive decline including dementia-Alzheimer syndrome (Dem-AD). The absence of a therapy to impede or postpone Dem-AD determines the need for its prevention, including nutritional factors. To evaluate the preventive capacity of M&D consumption in elderly Dem-AD we performed a systematic review in the main biomedical databases and information resources, but we present this study as a narrative review to discuss better the complexity of this subject. The elderly Dem-AD has a long pre-symptomatic period and the M&D intake has a widespread use. These determinants and the quality flaws of published studies impeach us to answer whether M&D consumption is preventive for Dem-AD. Moreover, two long Japanese cohorts suggest that M&D intake could prevent Dem-AD. Prospective cohorts beginning in midlife (or early life) could answer this question in the future.
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Affiliation(s)
- Félix Bermejo-Pareja
- Research Unit, University Hospital "12 de Octubre", Madrid. Chair "Alzheimer disease", Department of Medicine, Faculty of Medicine, Complutense University of Madrid, Spain
| | | | - Sara Llamas-Velasco
- Research Institute (Imas12), University Hospital "12 de Octubre," Madrid, Spain
| | - Ester Tapias-Merino
- Research Institute (Imas12), University Hospital "12 de Octubre," Madrid, Spain
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Gustafson DR, Bäckman K, Scarmeas N, Stern Y, Manly J, Mayeux R, Gu Y. Dietary fatty acids and risk of Alzheimer's disease and related dementias: Observations from the Washington Heights-Hamilton Heights-Inwood Columbia Aging Project (WHICAP). Alzheimers Dement 2020; 16:1638-1649. [PMID: 32715635 PMCID: PMC8409226 DOI: 10.1002/alz.12154] [Citation(s) in RCA: 48] [Impact Index Per Article: 9.6] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/13/2022]
Abstract
INTRODUCTION High dietary intake of long chain, polyunsaturated fatty acids is associated with lower Alzheimer's disease (AD) risk. METHODS Washington Heights-Hamilton Heights-Inwood Columbia Aging Project is a multiethnic, prospective observational study of aging and dementia among elderly (≥ 65 years). Dietary intake was measured using a food frequency questionnaire. Dietary short-, medium-, and long-chain fatty acid intakes were categorized by number of carbons and double bonds. Consensus AD diagnoses were made. Associations between AD risk and dietary fatty acid and cholesterol intakes were estimated using multivariable Cox proportional hazards regression models. RESULTS Of 2612 multiethnic women (67%) and men (baseline age 76.3 [6.4] years), 380 developed AD over an average 4.5 years follow-up. Lower risk of AD was associated with increasing intakes of docosahexaenoic acid (DHA; hazard ratio [HR] = 0.73, 95% confidence interval [CI]: 0.57 to 0.95, P = 0.018) and eicosapentaenoic acid (EPA; HR = 0.74, 95% CI: 0.57 to 0.95, P = 0.021), and longer AD-free survival (P < 0.05). DISCUSSION Higher intake of DHA and EPA are protective for AD.
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Affiliation(s)
- Deborah R. Gustafson
- Department of Neurology, State University of New York Downstate Health Sciences University, Brooklyn, New York, USA
- Department of Neurochemistry and Psychiatry, Neuropsychiatric Epidemiology Unit, at the Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden
| | - K. Bäckman
- Department of Neurochemistry and Psychiatry, Neuropsychiatric Epidemiology Unit, at the Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden
| | - N. Scarmeas
- Department of Neurology, The Gertrude H. Sergievsky Center, Taub Institute for Research in Alzheimer’s Disease and the Aging Brain, Columbia University and The New York Presbyterian Hospital, New York, New York, USA
- 1st Department of Neurology, Aiginition Hospital, National and Kapodistrian University of Athens Medical School, Athens, Greece
| | - Y. Stern
- Department of Neurology, The Gertrude H. Sergievsky Center, Taub Institute for Research in Alzheimer’s Disease and the Aging Brain, Columbia University and The New York Presbyterian Hospital, New York, New York, USA
| | - J.J. Manly
- Department of Neurology, The Gertrude H. Sergievsky Center, Taub Institute for Research in Alzheimer’s Disease and the Aging Brain, Columbia University and The New York Presbyterian Hospital, New York, New York, USA
| | - R. Mayeux
- Department of Neurology, The Gertrude H. Sergievsky Center, Taub Institute for Research in Alzheimer’s Disease and the Aging Brain, Columbia University and The New York Presbyterian Hospital, New York, New York, USA
- The Department of Epidemiology, Joseph P. Mailman School of Public Health, Columbia University, New York, New York, USA
| | - Y. Gu
- Department of Neurology, The Gertrude H. Sergievsky Center, Taub Institute for Research in Alzheimer’s Disease and the Aging Brain, Columbia University and The New York Presbyterian Hospital, New York, New York, USA
- The Department of Epidemiology, Joseph P. Mailman School of Public Health, Columbia University, New York, New York, USA
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Alzheimer's Disease as a Result of Stimulus Reduction in a GABA-A-Deficient Brain: A Neurocomputational Model. Neural Plast 2020; 2020:8895369. [PMID: 33123190 PMCID: PMC7582082 DOI: 10.1155/2020/8895369] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/24/2020] [Revised: 08/17/2020] [Accepted: 09/09/2020] [Indexed: 02/07/2023] Open
Abstract
Several research studies point to the fact that sensory and cognitive reductions like cataracts, deafness, macular degeneration, or even lack of activity after job retirement, precede the onset of Alzheimer's disease. To simulate Alzheimer's disease earlier stages, which manifest in sensory cortices, we used a computational model of the koniocortex that is the first cortical stage processing sensory information. The architecture and physiology of the modeled koniocortex resemble those of its cerebral counterpart being capable of continuous learning. This model allows one to analyze the initial phases of Alzheimer's disease by “aging” the artificial koniocortex through synaptic pruning, by the modification of acetylcholine and GABA-A signaling, and by reducing sensory stimuli, among other processes. The computational model shows that during aging, a GABA-A deficit followed by a reduction in sensory stimuli leads to a dysregulation of neural excitability, which in the biological brain is associated with hypermetabolism, one of the earliest symptoms of Alzheimer's disease.
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