JOURNAL/nrgr/04.03/01300535-202601000-00036/figure1/v/2025-06-09T151831Z/r/image-tiff Indicaxanthin is a betalain that is abundant in Opuntia ficus-indica orange fruit and has antioxidative and anti-inflammatory effects. Nevertheless, very little is known about the neuroprotective potential of indicaxanthin. This study investigated the impact of indicaxanthin on neuronal damage and gut microbiota dysbiosis induced by a high-fat diet in mice. The mice were divided into three groups according to different diets: the negative control group was fed a standard diet; the high-fat diet group was fed a high-fat diet; and the high-fat diet + indicaxanthin group was fed a high-fat diet and received indicaxanthin orally (0.86 mg/kg per day) for 4 weeks. Brain apoptosis, redox status, inflammation, and the gut microbiota composition were compared among the different animal groups. The results demonstrated that indicaxanthin treatment reduced neuronal apoptosis by downregulating the expression of proapoptotic genes and increasing the expression of antiapoptotic genes. Indicaxanthin also markedly decreased the expression of neuroinflammatory proteins and genes and inhibited high-fat diet-induced neuronal oxidative stress by reducing reactive oxygen and nitrogen species, malondialdehyde, and nitric oxide levels. In addition, indicaxanthin treatment improved the microflora composition by increasing the abundance of healthy bacterial genera, known as producers of short-chain fatty acids ( Lachnospiraceae , Alloprovetella , and Lactobacillus ), and by reducing bacteria related to unhealthy profiles ( Blautia , Faecalibaculum , Romboutsia and Bilophila ). In conclusion, indicaxanthin has a positive effect on high-fat diet-induced neuronal damage and on the gut microbiota composition in obese mice.

Depression and cardiometabolic conditions are suggested as modifiable risk factors for dementia, yet their combined impact remains unclear. This study assessed the independent and combined effects of depressive symptoms and cardiometabolic conditions on dementia incidence in England, the US and China.

The sample comprised 4472 participants aged 50 and older from the English Longitudinal Study of Ageing (ELSA), 5021 from Health and Retirement Study (HRS), and 8925 from China Health and Retirement Longitudinal Study (CHARLS). Depressive symptoms were assessed using the Center for Epidemiological Studies-Depression scale. Cardiometabolic factors included central obesity, low high-density-lipoprotein (HDL) cholesterol, systolic and diastolic blood pressure (BP), hyperglycemia, diabetes, and inflammation. Dementia incidence was estimated using confounder-adjusted Cox proportional hazards regressions, and pooled estimates were obtained using random-effects meta-analysis.

A total of 1218 individuals developed dementia over a median of 6.8-12.2 years. Depressive symptoms (ELSA: HR = 1.47 [95 % CI = 1.09-2.00]; HRS: HR = 1.68 [95 % CI = 1.33-2.13]; CHARLS: HR = 1.35 [95 % CI = 1.12-1.64]) and elevated systolic BP (ELSA: HR = 1.51 [95 % CI = 1.17-1.95]; HRS: HR = 1.48 [95 % CI = 1.24-1.79]; CHARLS: HR = 1.26 [95 % CI = 1.05-1.52]) were linked to dementia risk in all countries. While cardiometabolic multimorbidity (≥2 conditions) was not associated with dementia risk, those with the highest cardiometabolic index (≥4 conditions) had a greater risk of dementia in all samples (ELSA: HR = 1.82 [95 % CI = 1.01-3.26]; HRS: HR = 1.85 [95 % CI = 1.02-3.35]; CHARLS: HR = 1.65 [95 % CI = 1.18-2.30]).

Depressive symptoms are independently linked to dementia risk, while having multiple cardiometabolic conditions further increases this risk, especially when co-occurring with depressive symptoms in both Western and Chinese populations.

Tau protein is enriched in neuronal axons, it functions as a stabilizer of axonal transportation. Hyperphosphorylation of Tau in the brain results in early-onset Alzheimer's disease (AD), causes remarkable bone loss. Notably, pathological Tau leads to the loss of specific physiological Tau that exaggerates Tau toxicity. However, little was known about the physiological role of Tau in bone homeostasis although it's rarely expressed in peripheral tissues. Here, we provided evidence for brain Tau's role in promoting bone formation. Tau knockout (Tau-/-) mice showed smaller body size and exhibited osteoporotic-like deficit, including reduced trabecular and cortical bone mass, especially in young male Tau-/- mice. Such a deficit is likely due to a decrease in osteoblast (OB)-mediated bone formation, as little change in bone resorption in Tau-/- mice. Further mechanistic studies showed increased PPARγ signaling in the brain of Tau-/- mice, which contributed to chemerin release and CMKLR1upregulation in Tau-/- mice brain. Chemerin neutralization remarkably restored osteogenesis potential. Furthermore, reduced repressive H3K9me2 in Tau-/- mice brain led to decreased enrichment of H3K9me2 at PPARγ promoter and thus increased chemerin production. Moreover, PPARγ inhibitor GW9662 significantly reversed the osteoporotic phenotype of Tau-/- mice. Our results implicated brain Tau acting as a dominant positive regulator in bone mass, and unveiled a potential clinical value of PPARγ inhibition in treatment of AD-associated osteoporotic deficits.

Depression and anxiety coexist with Alzheimer's disease (AD) and Parkinson's disease (PD), yet their progression trajectories vary, necessitating a thorough examination of prescription patterns for antidepressants and anti-anxiety drugs pre- and post-diagnosis.

To systematically compare the prescriptions of antidepressant and anti-anxiety drugs across AD and PD over 10 years before and after initial diagnosis in the UK and France.

Data on 19,954 patients with AD, 25,267 with PD from the UK, 17,463 with AD, 10,333 with PD from France were extracted from The Health Improvement Network database. For both countries, we compared the odds of prescribed antidepressants and anti-anxiety drugs for each diagnosis group, over 10 years before and after diagnosis, using logistic regressions adjusting for age, sex, and drug prescriptions for chronic diseases.

Antidepressant prescriptions showed a significant rise from 25 % 5-10 years before the initial AD diagnosis to 50 % within the first 5 years post-diagnosis. AD Patients were more likely to be prescribed antidepressants than PD patients [Odds ratios ranging from 1.02 to 1.13 in the UK and 1.09-1.36 in France] and conversely PD patients were more likely to be prescribed anti-anxiety drugs [0.83-0.84 in the UK and 0.85-0.90 in France] several years before their diagnosis. AD patients sustained elevated antidepressant prescriptions up to 5 years after diagnosis.

These findings offer insights into disease-specific psychological impacts and underscore the necessity for further investigation into prescription patterns and their implications on patient outcomes.

On average, people with dementia fall more often than their age-matched peers, with serious consequences, yet the underlying reasons remain poorly understood. This narrative review explores relevant psychological, physiological and neuroimaging studies to discuss whether diminished inhibitory control contributes to poor balance and falls in people with Alzheimer's Disease (AD), the most common form of dementia. Inhibitory control, a component of executive function, plays a vital role in suppressing dominant impulses or actions and regulating attention in favour of a desired outcome. Although objective tests of inhibitory control are not routinely used in clinical settings, research suggests inhibitory control declines early, and progressively, in AD. Postural tasks that require inhibitory control can improve the accuracy of distinguishing fallers from non-fallers beyond known factors. Neuroimaging studies link the prefrontal cortex to both inhibitory and postural control, and this region exhibits neuronal loss early in AD. Thus, emerging evidence suggests that accurately assessing inhibitory control could not only improve falls risk predictions but also aid AD detection.

The study analyzed the association of area-level socioeconomic status (SES) with the risk of all-cause dementia, Parkinson's Disease (PD), and all-cause mortality using a multistate approach. Data from the UK Biobank were used (N = 363,663 50+y individuals, ≤15y follow-up), and Cox proportional hazards and multistate parametric models including Weibull regression were conducted, while cardiovascular health was tested as a potential mediator. In multistate models, socioeconomic area-level deprivation, measured by the Townsend Deprivation Index (TDI) z-score, was positively associated with the hazard of going from healthy into the 3 states of PD, dementia, and all-cause mortality (i.e. transitions 1: HR = 1.06, 95 % CI:1.02-1.10, P = 0.005, 2: HR = 1.19, 95 % CI: 1.16-1.22, P < 0.001 and 3: HR = 1.19, 95 % CI: 1.18-1.21, P < 0.001), with no association detected for transitions 4 (PD→Dementia), 5 (PD→Death), or 6 (Dementia→Death). Cardiovascular health did not mediate these associations. Socioeconomic area-level deprivation was directly associated with reduced survival rates from Healthy into Dementia, PD and Death.

Stroke, dementia, and late-life depression (LLD) are age-related brain diseases that pose significant public health challenges and costs. Leucocyte telomere length (LTL) is a biological aging marker influenced by both genetic and lifestyle factors. The aim of our study was to determine the association between LTL and these diseases. We further investigated whether modifying risk factors of age-related brain disease, as measured using the Brain Care Score (BCS), mitigates LTL associations.

We analyzed participants from the UK Biobank with available LTL and risk factor information. We examined LTL's associations with stroke, dementia, and LLD, individually and as a composite outcome, using continuous measures and tertile stratification. Disease risks were evaluated through cumulative incidence curves, incidence rates per 1,000 person-years, and adjusted Cox models. Risk comparisons across LTL tertiles were stratified by risk factor profiles, with high BCS (≥15) indicating healthier lifestyle choices and low BCS (≤10) reflecting less optimal lifestyle choices. Mendelian randomization (MR) was used to test causal associations.

The study included 356,173 participants (median age 56 years; 53.69% female). Shorter LTL was consistently associated with higher incidence rates across all outcomes. Participants in the shortest LTL tertile had elevated risks of the composite outcome (hazard ratio [HR] 1.11; 95% CI 1.08-1.15), stroke (HR 1.08; 95% CI 1.02-1.15), dementia (HR 1.19; 95% CI 1.12-1.26), and LLD (HR 1.14; 95% CI 1.09-1.18). Individuals with both shorter LTL and lower BCS faced significantly increased risks of age-related brain diseases (HR 1.11; 95% CI 1.07-1.16) and individually for stroke (HR 1.10; 95% CI 1.02-1.19), dementia (HR 1.17; 95% CI 1.08-1.28), and LLD (HR 1.13; 95% CI 1.07-1.19). Conversely, individuals with higher BCS within the shortest LTL group did not show a significant increase in risk of any age-related brain diseases. MR analyses did not identify causal relationships between LTL and these outcomes.

Individuals with shorter LTL are at increased risk of stroke, dementia, and LLD. Improved modifiable risk factor profiles seem to mitigate the impact of LTL on these diseases. Future research should explore the effectiveness of lifestyle interventions in mitigating adverse biological aging effects on brain health.

Diabetes mellitus has been shown to increase the risk of dementia, with diabetic patients demonstrating twice the dementia incidence rate of non-diabetic populations. We aimed to develop and validate a novel machine learning-based dementia risk prediction tool specifically tailored for diabetic population.

Using a prospective from 42,881 diabetic individuals in the UK Biobank, a rigorous multi-stage selection framework was implemented to optimize feature-outcome associations from 190 variables, and 32 predictors were final retained. Subsequently, eight data analysis strategies were used to develop and validate the dementia risk prediction model. Model performance was assessed using area under the curve (AUC) metrics.

During a median follow-up of 9.60 years, 1337 incident dementia cases were identified among diabetic population. The Adaboost classifier demonstrated robust performance across different predictor sets: full model with 32 predictors versus streamlined simplified model with 13 predictors selected through forward feature subset selection algorithm (AUC: 0.805 ± 0.005 vs. 0.801 ± 0.005; p = 0.200) in model development employing an 8:2 data split (5-fold cross-validation for training). To facilitate community generalization and clinical applicability, the simplified model, named DRP-Diabetes, was deployed to a visual interactive web application for individualized dementia risk assessment.

Some variables were based on self-reported.

A convenient and reliable dementia risk prediction tool was developed and validated for diabetic population, which could help individuals identify their potential risk profile and provide guidance on precise and timely actions to promote dementia delay or prevention.

The impact of adherence to low-risk lifestyle factors on dementia risk in individuals with obesity remains unclear. We aimed to explore the association between healthy lifestyles with dementia in obese participants.

Dementia-free participants from the UK Biobank, aged 50 years or older with obesity (BMI ≥30 kg/m2) at baseline were included. A weighted healthy lifestyle score was calculated incorporating both traditional and emerging lifestyle factors. The primary outcome was all-cause dementia and its subtypes (Alzheimer's disease and Vascular dementia). Cox regression models analyzed the association between healthy lifestyle scores and dementia risk. Restricted cubic splines tested the dose-response. We also examined the effect of lifestyle scores on dementia risk in individuals with normal weight and overweight.

A total of 54,365 participants were included at baseline. During a median follow-up of 14.4 years, 1271 participants developed all-cause dementia, including 537 cases of Alzheimer's disease and 343 cases of vascular dementia. A 20 % increase in the lifestyle score was associated with a 7 % reduction in dementia risk (HR: 0.93; 95 % CI: 0.91,0.96) and a 4 % reduction in Alzheimer's disease risk (HR: 0.96; 95 % CI: 0.92,1.00). The association was stronger in overweight and obese participants. No significant link was found for vascular dementia.

Information on lifestyle behaviors was self-reported and might be prone to measurement error.

Adherence to a healthy lifestyle may reduce the risk of dementia and Alzheimer's disease in older obese individuals, with a stronger effect observed in those with higher lifestyle scores.

Many countries face an unprecedented challenge in aging demographics. This has led to an exponential growth in research on aging, which, coupled to a massive financial influx of funding in the private and public sectors, has resulted in seminal insights into the underpinnings of this biological process. However, critical validation in humans has been hampered by the limited translatability of results obtained in model organisms, additionally confined by the need for extremely time-consuming clinical studies in the ostensible absence of robust biomarkers that would allow monitoring in shorter time frames. In the future, molecular parameters might hold great promise in this regard. In contrast, biomarkers centered on function, resilience, and frailty are available at the present time, with proven predictive value for morbidity and mortality. In this review, the current knowledge of molecular and physiological aspects of human aging, potential antiaging strategies, and the basis, evidence, and potential application of physiological biomarkers in human aging are discussed.

Liver fat is associated with cardiometabolic disease, cerebrovascular disease, and dementia. Cerebrovascular disease, most often cerebral small vessel disease, identified by magnetic resonance imaging as white matter hyperintensities (WMHs) often contributes to dementia. However, liver fat's role in the relationship between cardiometabolic risk, WMHs, and cognitive performance is unclear.

In the UK Biobank cohort (N = 32,461, 52.6% female; mean age 64.2 ± 7.7 years; n = 23,354 in the cognitive performance subsample), we used linear regression to investigate associations between cardiometabolic factors measured at baseline and liver fat, WMHs, and cognitive performance measured at follow-up, which was 9.3 ± 2.0 years later on average. We used structural equation modeling to investigate whether liver fat mediated associations between cardiometabolic factors and WMHs and whether WMHs mediated associations between liver fat and cognitive performance.

Nearly all cardiometabolic factors were significantly associated with liver fat (|r| range = 0.03-0.41, p = 3.4 × 10-8 to 0) and WMHs (|r| = 0.04-0.15, p = 5.8 × 10-13 to 7.0 × 10-159) in regression models. Liver fat was associated with WMHs (r = 0.11, p = 4.3 × 10-82) and cognitive performance (r = -0.03, p = 1.6 × 10-7). Liver fat mediated the associations between cardiometabolic factors and WMHs (|βmediation| = 0.003-0.027, p mediation = 1.9 × 10-8 to 0), and WMHs mediated the associations between liver fat and cognitive performance (βmediation = -0.01, p mediation = 0).

Our findings indicate that liver fat mediates associations between cardiometabolic factors and WMHs and that WMHs mediate the association between liver fat and cognitive performance. This suggests that liver fat may be important for understanding the effects of cardiometabolic factors on cerebrovascular disease and cognitive function. Experimental studies are warranted to determine relevant targets for preventing vascular-driven cognitive impairment.

Accurately estimating one-year mortality risk in older women with dementia can inform clinical decision-making, facilitate timely advanced care planning, and optimise palliative care delivery. This study aimed to develop, validate, and assess the clinical utility of a prediction model for one-year all-cause mortality in this population using a nationally representative Australian cohort.

This prognostic study utilised data from the 1921-26 cohort of the nationally representative, population-based Australian Longitudinal Study on Women's Health (ALSWH) and linked national and state-based administrative health records. Candidate predictors were identified through a systematic review and expert consultation, then refined using a data-driven statistical approach. A multivariable binary logistic regression model was developed and validated to predict one-year all-cause mortality.

The analysis included 1576 older women with dementia (mean age, 72.6 ± 1.5 years). The model demonstrated good discrimination (AUC: 75.1 %, 95 % CI: 72.7 %-77.5 %) and excellent calibration (slope = 1.00, 95 % CI: 0.87-1.13; intercept = 0.00, 95 % CI: 0.11 - 0.11). Model validation using both 10-fold cross-validation and 1000 bootstrap iterations showed minimal optimism in its predictive performance, with AUC optimism of 0.0047 and 0.0042, respectively. Decision curve analysis indicated a net benefit across probability thresholds from 0.24 to 0.88, supporting the model's clinical utility for guiding palliative care decisions.

This prediction model, incorporating readily available predictors, demonstrated compelling performance and clinical utility for identifying older women with dementia at high risk of one-year mortality. The model has the potential to facilitate timely palliative care interventions and is publicly accessible via a web-based calculator. Further external validation in diverse populations and healthcare settings is warranted to confirm its generalisability.

Recent evidence from a quasi-experiment in Wales showed that herpes zoster (HZ) vaccination appears to prevent or delay dementia. Exploiting a similar quasi-experiment in Australia, this study investigated the effect of HZ vaccination on dementia occurrence in a different population and health system setting.

To determine the effect of HZ vaccination on the probability of receiving a new diagnosis of dementia.

In Australia, starting November 1, 2016, live attenuated HZ vaccination was provided free to individuals aged 70 to 79 years through primary care clinicians. Thus, individuals whose 80th birthday was just a few weeks before November 1, 2016, never became eligible, whereas those whose 80th birthday was just a few weeks later were eligible. The key strength of this quasi-experiment is that one would not expect that these comparison groups who differ in age only minutely would, on average, differ in any health characteristics and behaviors. Primary health care records were analyzed with week-of-birth information from 65 general practices across Australia, using a regression discontinuity design.

Eligibility for HZ vaccination based on date of birth.

New diagnoses of dementia as recorded in primary care electronic health record data.

In this sample of 101 219 patients, 52.7% were women and mean age was 62.6 years (SD, 9.3 years) as of November 1, 2016. Individuals born just before vs just after the date-of-birth eligibility threshold (November 2, 1936) for HZ vaccination were well balanced in their past preventive health services uptake and past chronic disease diagnoses. There was an abrupt increase of 16.4 percentage points (95% CI, 13.2-19.5; P < .001) in the probability of ever receiving HZ vaccination between patients born shortly before vs shortly after the date-of-birth eligibility threshold. The eligibility rules of the HZ vaccination program thus created comparison groups born just on either side of the date-of-birth eligibility threshold who were likely similar to each other, except for a large difference in their probability of receiving the intervention (HZ vaccination) of interest. This study found that eligibility for HZ vaccination (ie, being born shortly after vs shortly before November 2, 1936) decreased the probability of receiving a new dementia diagnosis during 7.4 years by 1.8 percentage points (95% CI, 0.4-3.3 percentage points; P = .01). Being eligible for HZ vaccination did not affect the probability of taking up other preventive health services (including other vaccinations) or the probability of receiving a diagnosis of common chronic conditions other than dementia.

By taking advantage of a quasi-experiment and corroborating findings from Wales in a different population, this study provides evidence of the potential benefits of HZ vaccination for dementia that is more likely to be causal than that of more commonly conducted associational studies.

The prevalence of cognitive impairment (CI) is progressively rising. Insufficient awareness, complex diagnostic procedures, and the absence of effective treatment methods contribute to the challenge. Therefore, our objective is to develop and validate a CI screening model specifically for the elderly population in China.

The multi-center cross-sectional study included 18 communities in four provinces, and data collection was performed on basic parameters, medical history, physical measurements, cognitive assessments, and blood sample tests. The least absolute shrinkage and selection operator (Lasso) and multiple-factor logistic regression analysis were used to select variables with best predictive performance to build the model that minimizes the mean squared error and build a nomogram of the CI screening model. The Receiver Operating Characteristic (ROC) curve, calibration curve, decision curve analysis (DCA), and clinical impact curve (CIC) are utilized to assess the discriminative ability and clinical utility of the model. Both internal and external datasets are utilized for model validation.

The development set of the model included a total of 1,479 participants, among whom 278 were identified as having cognitive impairment (CI), with a prevalence of 18.8%. Eight predictive factors for CI were selected as the final model, including age, falls times in 1-year, educational level, place of residence, hypertension, stroke, protein intake, and subcutaneous fat loss. The area under the curve (AUC) of the model was 0.873, indicating good discriminative ability. The calibration curve demonstrated good consistency between predicted and observed results. DCA and CIC analysis showed that the model had favorable clinical utility. The AUC, calibration curve, DCA, and CIC of both internal and external validation sets showed consistent results with the development set, indicating good consistency.

We developed an accurate and valid nomogram of CI screening with all the required factors easily available and four of them modifiable.

This study investigated the effects of work cessation on cognitive function among older adults in rural China. Given that cognitive disorders affect 6.04% of individuals aged 60 and above-with higher prevalence in rural areas-understanding this relationship is critical.

A cross-sectional study was employed, using data from the 2020 wave of the China Health and Retirement Longitudinal Study (CHARLS). Regression analysis assessed the impact of work cessation on cognitive function and the moderating effects of social activities, health behaviours and internet use.

Data were collected from 150 districts, 450 villages, and urban community units in China.

The study included 6,318 participants, with 4,045 currently employed and 2,273 no longer working.

Cognitive function was evaluated using measures of mathematical computation, temporal and image cognition, and situational memory was tested through 20 memory-related questions. Explanatory variables included work cessation status, while moderating variables encompassed social activities, health behaviours (smoking and alcohol consumption) and internet use.

Work cessation has a negative impact on cognitive function, particularly situational memory and overall cognitive ability. Stopping work was associated with a decrease in cognitive functioning by 0.796 SD (p<0.01), a reduction in situational memory capacity by 1.083 SD (p<0.01) and a decline in total cognitive ability by 1.879 SD (p<0.01). However, more social activities, better health behaviours (eg, quitting smoking) and internet use can alleviate the impact. Seniors with high social activity levels showed an increase in cognitive functioning by 0.375 SD (p<0.01), while those who drank less alcohol had a 0.598 SD improvement in cognitive functioning (p<0.01). Internet use improved cognitive function by 1.265 SD (p<0.01).

Work cessation significantly reduced cognitive function in rural Chinese older adults. Leisure activities can mitigate this decline, but they often lack quality and diversity. Health behaviour improvements show heterogeneity, and internet use mitigates cognitive decline despite urban-rural digital gaps. To protect rural older adults' cognitive function, policies promoting flexible employment, enhanced recreational infrastructure, health outreach and bridging digital divides are proposed.

Our study assesses the association between cumulative handgrip strength and longitudinal changes in cognitive function and daily functioning.

Two comparative cohort studies were used, including the English Longitudinal Study of Ageing (ELSA) and the Survey of Health, Ageing and Retirement in Europe (SHARE). Cumulative handgrip strength was calculated using three repeated measurements of handgrip strength. Linear mixed regression models evaluated the association between cumulative handgrip strength and longitudinal changes in cognitive function and daily functioning. Cox regression models were performed to determine the association between cumulative handgrip strength and the risk of cognitive and functional impairment.

Individuals with lower levels of cumulative handgrip strength had lower global cognition (β: -0.244; 95% CI: -0.317, -0.170 for ELSA and -0.359; -0.406, -0.311 for SHARE) and experienced a faster decline in cognitive function over time (-0.025; -0.037, -0.013 for ELSA, and -0.019; -0.026, -0.013 in SHARE). We found lower levels of cumulative handgrip strength were associated with lower daily functioning (β: 0.267; 95% CI: 0.161, 0.374 for ELSA and 0.153; 0.079, 0.227 for SHARE), and a faster decline in daily functioning over time (0.105; 0.081, 0.129 for ELSA and 0.217; 0.195, 0.238 for SHARE). Furthermore, lower levels of cumulative handgrip strength were related to a higher risk of cognitive and functional impairment.

Our study suggested that lower levels of cumulative handgrip strength was related to an accelerated decline in cognitive function and daily functioning. Persistently strengthening muscle strength should be emphasized in preventing neurodegenerative disorders and disabilities.

There is evidence of increased risk of cognitive disability due to short sleep duration and adverse Social Determinants of Health (SDoH). To determine whether spatial associations (correlation between spatially distributed variables within a given geographic area) exist between neighborhoods with short sleep duration and cognitive disability across the United States (US) after adjusting for other factors. We conducted a spatial analysis using a spatial lag model at the neighborhood-level with the census tract as unit-of-analysis within each state in the US. We aggregated our results nationally using a weighted analysis to adjust for the number of census tracts per state. This study used Centers for Disease Control and Prevention (CDC) data on short sleep duration, cognitive disability and other health factors. We used 2021-2022 neighborhood-level data from the CDC and US Census Bureau adjusting for social determinants of health (SDoH) and demographics, excluding Florida due to inconsistencies in data availability. Our exposure variable was self-reported short sleep defined by the CDC ("sleep less than 7 hours per 24 hour period"). Our outcome was self-reported cognitive disability defined by the CDC ("difficulty concentrating, remembering, or making decision"). We adjusted for other factors including 'health outcomes', 'preventive practices', and the CDC's Social Vulnerability Index.

The spatial analysis revealed a significant association between short sleep duration and an increased risk of cognitive disability across the US (estimate range [0.29; 1.27], p < 0.005) after adjustment. Notably, six Western states (New Mexico, Alaska, Arizona, Nevada, Idaho, and Oregon) were at increased risk of cognitive disability due to short sleep duration and this pattern was significant (p = 0.007).

Our study highlights the importance of short sleep duration as a significant predictor of cognitive disability across the US after adjusting for other confounders. The association between short sleep and cognitive disability was especially strong in the Western region of the US providing a deeper understanding of how geographic context and local factors can shape health outcomes.

Aging-associated cognitive decline affects more than half of those in long-term residential aged care. Emerging evidence suggests that gut microbiome-host interactions influence the effects of modifiable risk factors. We investigated the relationship between gut microbiome characteristics and severity of cognitive impairment (CI) in 159 residents of long-term aged care. Severe CI was associated with a significantly increased abundance of proinflammatory bacterial species, including Methanobrevibacter smithii and Alistipes finegoldii, and decreased relative abundance of beneficial bacterial clades. Severe CI was associated with increased microbial capacity for methanogenesis, and reduced capacity for synthesis of short-chain fatty acids, neurotransmitters glutamate and gamma-aminobutyric acid, and amino acids required for neuroprotective lysosomal activity. These relationships were independent of age, sex, antibiotic exposure, and diet. Our findings implicate multiple gut microbiome-brain pathways in aging-associated cognitive decline, including inflammation, neurotransmission, and autophagy, and highlight the potential to predict and prevent cognitive decline through microbiome-targeted strategies.

The microbiome plays a critical role in both promoting human health and contributing to diseases. Multiple emerging evidence shows that it contributes to aging and cognitive decline; however, the mechanisms are not fully understood. Changes in the microbiome and immune system occur with age, and immune functions are one of the key mechanisms linking the microbiome to the brain. Disrupted immunological balance may lead to neuroinflammation and blood-brain barrier dysfunction, contributing to cognitive decline. However, comprehensive knowledge regarding the types of microbiome and immune interactions influencing neuronal and cognitive health in aging remains largely unknown. This review presents evidence about the types of microbiome alterations associated with healthy versus unhealthy aging and how they interact with immune cells linked to neuronal and cognitive functions. It also explores whether and how microbiome modulators like probiotics, prebiotics, and postbiotics can be potential interventions to help preserve cognitive function in older adults.

Education is among the most robust predictors of cognitive health outcomes in later life. However, few studies have comprehensively evaluated whether and how much of this effect is explained by occupational exposures. This study aims to determine if and how much pre-retirement occupational exposures (occurring before age 60) mediate the association between education and cognitive function at age 65+.

We use data drawn from the Health and Retirement Study (HRS) and Occupation Information Network (O*NET) data. Informed by previous research and theory, we conducted Confirmatory Factor Analyses of occupation-level exposure measures using a longitudinal HRS-O*NET linked data set we created, and we identified 2 latent factors: occupational hazards and occupational complexity. Among initially employed adults (age 51-60 at baseline), we used Structural Equation Modeling (SEM) to evaluate the association between education and cognitive function at age 65+, and the role of our 2 occupational factors in mediating this association.

The measurement and structural models both had good model fit (TLI, CFI ≥ 0.95, SRMR < 0.08). We found (a) that education remained a critical predictor of cognitive outcomes in later life even when accounting for occupational exposures, and (b) only hazardous exposures mediated the association between education and cognitive function in later life (a2b2=0.02, p = .01), explaining about 17% of the effect of education.

These findings suggest interventions designed to decrease exposure to hazardous occupational exposures could reduce some of the cognitive disadvantages in later life associated with lower levels of education.

Obesity is a modifiable dementia risk factor, but body mass index does not account for fat distribution, particularly visceral fat, which is more strongly linked to metabolic and cardiovascular health. Despite its relevance, research on visceral fat and dementia is limited, especially in large-scale prospective studies. The aim of this study was to assess the association between visceral fat and dementia risk, its interaction with genetic predisposition, and the impact of healthy lifestyle adherence.

Using data from the UK Biobank (UKB) cohort, we computed baseline, sex-specific visceral fat percentage (VFP), defined as the ratio of visceral fat mass to total body fat mass. Nonlinear associations between VFP and incident dementia were initially assessed using restricted cubic splines. The relationship between VFP and incident dementia was further examined using Cox proportional hazard models. In addition, stratified and interaction analyses were conducted to assess dementia incidence across VFP levels, lifestyle factors, and genetic risk.

The study included 63,042 women (mean age: 63.96 years) and 74,001 men (64.20 years) aged 60 years and older from the UKB, with a median follow-up of 14.07 years for men and 14.09 years for women. During follow-up, 2,805 men and 1,893 women developed dementia. A U-shaped association between VFP and dementia risk was observed in both sexes. In men, each SD increase in VFP below the median value of 8.1% was associated with a reduced risk of dementia (HR: 0.90, 95% CI 0.85-0.96), whereas above the median, the risk increased (1.06, 1.00-1.11). Similarly, in women, below the median VFP value of 3.1%, each SD increase was linked to a decreased dementia risk (0.89, 0.83-0.96), and above the median, the risk increased (1.14, 1.07-1.22). No significant interactions were found between VFP and genetic risk or lifestyle factors.

Among nondemented, community-dwelling older Britons, atypical VFP was associated with higher dementia risk in both sexes. The lack of interaction between VFP and genetic risk highlights the complexity of dementia pathogenesis. In addition, a healthy lifestyle may mitigate the dementia risk associated with atypical VFP levels.

Device-based sedentary time shows a nonlinear association with incident dementia among older adults. However, associations between sedentary time and cognitive performance have been inconsistent. We examined potential nonlinear associations between sedentary time and performance on cognitive tests among older adults.

We used data from the UK Biobank and included 32,875 adults aged 60-79. Sedentary time was estimated from a machine learning-based analysis of 1 week of wrist-worn accelerometer data. The primary outcomes were performance on 6 cognitive tests completed online (fluid intelligence test, short-term numeric memory test, symbol substitution test, visual-spatial memory test, alphanumeric, and numeric trail making tests), as well as a composite cognitive score.

Except for the visual-spatial memory test, nonlinear approaches provided a better fit than linear methods to model the associations of sedentary time with other cognitive outcomes. For these outcomes, segmented regression models showed that, although effect sizes were small, higher sedentary time was associated with better cognitive performance up to a threshold of sedentary time that varied from 9.7 to 12.3 hr per day. Above this threshold, the association between sedentary time and cognitive performance was attenuated toward the null or became negative (for the symbol substitution test only).

As accounted by our nonlinear approach, the association between sedentary time and cognitive performance may shift from positive to null or negative above a 10-12-hr threshold among older adults. A combination of device-based and self-report assessments of sedentary behavior is needed to better understand these nonlinear associations.

This study aimed to compare the effects of four structured exercise interventions-Tai Chi, Baduanjin, square dance, and Latin dance-on cognitive function, physical health, body composition, and psychosocial outcomes in older adults.

A 12-week randomized controlled trial (RCT) was conducted with 150 older adults aged 60 to 80 years (mean age: 69.7 ± 5.8 years; 62.7% female). Participants were assigned to one of five groups: Tai Chi, Baduanjin, square dance, Latin dance, or a health education control group. Pre- and post-intervention assessments included cognitive function (Montreal Cognitive Assessment, MoCA), upper limb strength (30-s arm curl test), flexibility (sit-and-reach test), balance (single-leg standing time), agility (2.4-m agility test), body fat percentage, and waist-to-hip ratio. Additionally, social interaction and psychological well-being were measured through standardized scales.

Significant improvements in cognitive function were observed in the square dance and Tai Chi groups (MoCA score increases of 4.2 and 3.7 points, respectively; p < 0.05). Square dance also led to notable improvements in grip strength (p < 0.01) and aerobic endurance (p < 0.05), while Latin dance showed the greatest benefits in flexibility and body fat percentage reduction. Psychological well-being improved across all intervention groups compared to the control group (p < 0.05), suggesting a broader impact on mental health and social engagement.

These findings indicate that structured physical activity interventions significantly enhance cognitive and physical health in older adults, with variations in effectiveness based on exercise type. Furthermore, the inclusion of social components in certain activities, such as square dance, may amplify cognitive benefits through increased engagement and reduced social isolation.

This study explored the views and opinions of individuals living with dementia, caregivers, and healthcare professionals on assistive technologies that facilitate independent living. Using a qualitative approach, the researchers conducted focus groups with 35 participants in England. Findings revealed both the benefits and limitations of technologies like medication management devices, activities of daily living aids, GPS tracking, and smart home systems. While participants recognized the potential to enhance independence and safety, they highlighted usability, reliability, and technological failure as significant challenges. The complexity of digital interfaces and the cognitive demands of online interactions emerged as key barriers. Participants expressed a strong desire for more adaptive, user-friendly, and responsive technologies. The study underscores the importance of user-centered design and collaboration between developers, caregivers, and people living with dementia. By addressing the identified issues, future assistive technologies can improve quality of life for individuals living with dementia and their caregivers. These insights can guide the development of more effective, accessible, and ethical assistive technologies in dementia care.

Cognitive decline often follows human immunodeficiency virus (HIV) infection. The objective of this study was to explore the factors present at HIV diagnosis associated with the risk of incident dementia.

A longitudinal observational study was conducted using a nationwide claim database (2008-2021). A cohort was designed using new diagnosis of HIV infection with antiretroviral therapy. Included in the analysis were individuals aged over 40, with > 3-year follow-up and without a diagnosis of dementia within 2 months post-HIV diagnosis. Dementia was defined as diagnosis and prescription of anti-dementia medication. Cox proportional hazards regression models assessed the association between baseline characteristics and the risk of incident dementia.

Among the 13,289 HIV-infected cohort, 3,929 met the inclusion criteria. The median age was 45 (interquartile range [IQR], 15), and 90.9% were male. During the median follow-up period of 7.6 (IQR, 5.0) years, dementia developed in 114 patients, with cumulative incidence reaching 4% at the 10-year follow-up. The development of dementia was associated with age at diagnosis ≥ 50 (hazard ratio [HR], 2.31; 95% confidence interval [CI], 1.51-3.53), low socioeconomic status (HR, 3.50; 95% CI, 2.22-5.52), and acquired immune deficiency syndrome (AIDS) status at diagnosis (HR, 2.05; 95% CI, 1.38-3.03).

This study underscores the importance of age at HIV diagnosis, socioeconomic status, and AIDS status as determinants of the risk of incident dementia among people living with HIV.

Sodium-glucose co-transporter 2 inhibitors have demonstrated potential for improving cognitive function in preclinical studies; however, robust clinical evidence supporting this effect in humans remains limited. We conducted a prospective trial to assess the effect of dapagliflozin on cognitive function in middle-aged and older patients with type 2 diabetes mellitus (T2DM) and mild cognitive impairment (MCI). Ninety participants were randomly assigned to either the dapagliflozin or control group for 36 weeks. Cognitive function was evaluated using the Montreal Cognitive Assessment (MoCA) and Mini-Mental State Examination (MMSE). Eight participants from each group underwent resting-state functional magnetic resonance imaging to assess region homogeneity (ReHo). After 36 weeks, the dapagliflozin group demonstrated significant improvements in MoCA and MMSE scores compared to the control group. Additionally, the dapagliflozin group exhibited reductions in diastolic blood pressure, glycated haemoglobin, fasting plasma glucose, homeostasis model assessment of insulin resistance (HOMA-IR), total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), and ReHo values in the left superior temporal gyrus were significantly reduced (p < 0.05). Spearman's correlation analysis revealed that improvements in MOCA scores before and after treatment were negatively correlated with HOMA-IR (r=-0.653, p=0.006), TC (r=-0.619, p=0.011), and ReHo values in the left superior temporal gyrus (r=-0.710, p=0.002) in both groups. These findings suggest that dapagliflozin may improve cognitive function and modulate ReHo values in the left superior temporal gyrus in middle-aged and older adults with T2DM. These effects may be linked to improvements in insulin sensitivity and reductions in TC.

Poor social networking (SN) is associated with the development of cognitive impairment and dementia. Our objective was to perform a systematic review of the evidence on the associations between SN and the incidence of dementia, disease pathology, level of cognition, and brain structure. Bibliographic databases (PubMed, Embase, Cochrane Library, CINAHL) and additional sources (Open Gray, Google Scholar, manual searches) were screened through November 30, 2024. Observational studies assessing the SN-dementia link were selected, with data extraction and bias evaluation performed independently by two authors via the PRISMA checklist and Newcastle-Ottawa Scale. We included 17 observational studies (355 initially screened), involving 20,678 participants aged 40-90 years, published between 2000 and 2024. Studies have utilized various SN assessment tools and cognitive measures, including the MMSE and MoCA. Poor SN was consistently associated with increased risks of dementia, cognitive decline, and severe disease pathology, particularly Alzheimer's disease (AD). Larger and more integrated SNs were linked to better cognitive resilience and lower conversion rates from mild cognitive impairment (MCI) to dementia. One study on frontotemporal dementia (FTD) indicated that the SN might mitigate cortical atrophy. SN size and density are also correlated with favorable structural brain changes, such as greater gray matter volume. This review highlights SN as a modifiable factor in dementia risk. However, its role in non-AD dementia, particularly FTD, requires further investigation. Future research should include more culturally diverse and methodologically robust studies. Randomized controlled trials will be important to determine whether intervention to expand social networks decreases incidence of progression of dementia.

Regulating stress effectively has a profound impact on our well-being and is known to be significantly interrelated to our social connections, as well as healthy lifestyle behaviors. However, the complex mechanisms through which these components are associated with maintaining well-being remain enigmatic. We propose a theoretical interrelated framework for which the maintenance of brain health assumes a central role. This involves the adaptive functionality of neural circuits associated with regulating emotions, self-control, and the ability to derive pleasure from rewards or enjoyable experiences. As a result, based on brain health as a central condition, we explore how different dimensions of social connections directly impact stress regulation, or indirectly through brain health. Furthermore, we delve into how lifestyle choices indirectly affect stress regulation, mediated by their impact on brain health. Reciprocally, our lifestyle choices are wired by our social connections, reinforcing the significant role of brain health. In the context of this conceptual framework, it is emphasized that psychotherapeutic interventions need to expand beyond the sole concentration on psychological processes. It is imperative to focus on interconnected biopsychosocial components known to positively enhance brain health, and hence to enhance the capacity of psychotherapy to significantly amplify mental health and well-being.

The COVID-19 pandemic has underscored the impact of social isolation on mental well-being. This study aims to evaluate the emotional and cerebral consequences of social isolation and assess whether prior environmental enrichment can mitigate the adverse effects. For that purpose, four groups were established: Behaviour group (Beh), n=8, subjected to a 4 % sucrose consumption test and the elevated zero maze (EZM) to assess anhedonia and unconditioned anxiety; Social isolation (SI) + Behaviour group, n=8, subjected to 4 consecutive weeks of social isolation followed by the behavioural testing; Environmental enrichment: EE+SI + Behaviour group, n = 8, subjected to EE prior to SI followed by behavioural assessment; and Basal group (BG), n = 8, used to determine the baseline of cytochrome c-oxidase (CCO). After behavioural testing, brain tissue from the prefrontal cortex (PFC), dorsal and ventral hippocampus (vHIP), nucleus accumbens (NAc), and ventral tegmental area (VTA) were analysed for CCO activity. Results show that SI serves as a significant stressor, increasing anxiety and anhedonic responses in the SI group. However, pre-exposure to EE significantly reduced these responses. Regarding CCO activity, the SI group exhibited elevated levels across all brain regions compared to the EE+SI group. Moreover, the EE+SI group maintained CCO activity levels similar to those of the Basal group, suggesting that prior EE exposure mitigates the metabolic impact of social isolation across most brain regions, except for the vHIP. These results indicate that pre-exposure to an EE may buffer the adverse effects of SI, supporting enhanced resilience.

Alzheimer's Disease (AD) is characterized by the formation of amyloid-β (Aβ) in the extracellular region, neurofibrillary tangles (NFTs) in the intracellular region accompanied with neuroinflammation and decreased neurotransmitters in various regions of brain leading to neuroinflammation and neurodegeneration. Of the various bioactive molecules, Cyclic Peptides (CPs) are small circular chains of amino acids that can alter the structure and function of the proteins they interact with. They can be synthesized using chemical or genetic approach leading to the generation of diverse libraries of CPs that are screened for binding with desired target proteins. In AD, CPs can interfere at various levels, by either imitating the structure or altering the conformation of amyloidogenic proteins. They can also interfere with signal transduction by competing with amyloid proteins for various receptors which are involved in AD pathology. This review highlights the application of CPs as scaffolds for the identification of novel small molecules that can interfere with amyloid aggregation or for the formulation of vaccination against AD. Other proteins involved in the pathophysiological pathways of AD that can potentially be targeted for CP design have also been discussed.

Visual impairment (VI) is prevalent in older adults and associated with cognitive decline. However, the mechanisms through which visual impairment affects cognitive functioning during the aging process are poorly understood. Our study aims to estimate the direct effect of visual acuity on cognitive function and its indirect effect through social isolation and depressive symptoms by sex and age.

Cross-sectional study.

117,231 individuals aged 40-70 participated in the UK Biobank baseline and ocular assessment. Of these, 81% were white, 54% were female, and 45.6% were aged 60-70. The mean age was 56.8 (SD 8.1) years.

Path analyses with multiple equations were conducted to examine the direct and indirect effects of visual acuity (VA). Stratified analyses by gender and age were performed.

LogMAR VA was the exposure, with social isolation and depressive symptoms as mediators. Cognitive functions, including visual memory, verbal-numerical reasoning, processing speed, and prospective memory, were the outcomes.

VA had a direct effect on cognitive function (β = -0.979 for reasoning and OR = 0.67 for prospective memory). VA also influenced cognition indirectly through social isolation and depressive symptoms. The direct effect of VA on cognitive function was similar in men vs. women and middle-aged vs. older. However, there is a marked difference in the mediating effect via social isolation and depressive symptoms by age and sex. The mediating effect of VI on cognition via social isolation was stronger in older adults than middle-aged and in men than women; while the mediating effect via depressive symptoms was stronger in women and middle-aged individuals. VI had the largest mediating effect via social isolation in older males.

Vision, social isolation, and depressive symptoms are modifiable factors and can be treated to preserve cognition. Encouraging social engagement among male and older adults with VI and promoting mental health awareness in women and middle-aged individuals with VI will reduce the negative impact of VI on cognition, lower dementia risk, and improve the well-being of aging adults.

Hearing in the elderly: Employees' perspectives on hearing care in long-term care facilities. A qualitative study Abstract: Background: Hearing impairment is common among the elderly. More than half of individuals 80 years and older exhibit severe hearing loss, and few retain good hearing performance. This impairment significantly affects both community participation and nursing care. Aim: This study aimed to examine the impact of hearing impairment on everyday life of employees and residents at long-term care facilities. We further sought to identify how employees perceive hearing care in order to identify potential for improvement. Methods: This sub-project of a larger study comprised guided focus groups with employees of long-term care facilities. The sample included six focus groups of nurses and nursing care assistants from long-term care facilities (n = 42). Collected data were analyzed using qualitative content analysis. Results: Hearing impairment hinders elderly resident participation in the nursing process and complicates daily communication between residents and nursing staff. Hearing impaired residents are less able to take part in group activities and tend to withdraw from the community. Lack of an effective hearing support structure renders hearing care services inaccessible to some residents. Conclusions: Optimized service structures, targeted assistance and training opportunities for employees specific to hearing impairment can provide sustainable hearing care for the elderly.

The study examines the association between social determinants of health, tooth loss, and cognitive decline. Using regression models, the 2020 Behavioral Risk Factor Surveillance data examined the study objective; it included 32,663 older adults who reported on cognitive status. Results suggested that older adults missing more than five teeth or unable to work are 1.61 times and 6.84 times more likely to report cognitive decline, respectively. Older adults with higher education and higher household incomes are less likely to report cognitive decline. Results suggested that older adults with no diabetes or who never smoked are 31% and 39% less likely to report a cognitive decline. The results suggested a significant association between tooth loss and cognitive decline among social determinants of health. A comprehensive approach to affect cognitive decline should include oral and social health strategies.

Advance care planning (ACP) is relevant yet challenging with cognitive decline.

To provide evidence and consensus-based clinical recommendations for how to conduct ACP in dementia.

International Delphi study conducted by the European Association for Palliative Care 'ACP in dementia' taskforce with four online surveys (September 2021-June 2022). A panel of 107 experts from 33 countries and seven individuals with dementia contributed. The recommendations specific for dementia were initially based on two earlier Delphi studies and literature searches addressing guidance including the right timing and how to personalize ACP. We used conservative preregistered criteria for consensus.

Thirty constitutive elements of ACP were identified (e.g., 'assess understanding of ACP'). Only five were deemed 'optional.' The panel estimated a median of four conversations could address elements to be addressed at least once. Recommendations included to assume capacity as a principle, conscious of the need to explore its fluctuation, to encourage engaging and playing active roles, and to establish connection and inform and prepare family. There was a consensus to offer ACP around dementia diagnosis, to raise end-of-life issues later, and to personalize ACP with flexibility, providing of information and exploring understanding. The advice of the persons with dementia pointed to a wish for a well-coordinated holistic approach.

Consensus was reached, including in areas of ambiguity, to guide ACP in dementia. ACP should be embedded in a nonprescriptive, individualized approach that involves both the person with dementia and their families. Future studies may evaluate trade-offs between optimal ACP and feasible implementation.

This study investigated the association between dietary potassium intake and cognitive function in older adults.

We conducted a cross-sectional observational study using data from the National Health and Nutrition Examination Survey (NHANES) 2011-2014. A total of 2555 participants, aged 60 years and older, were included in the analysis. Dietary potassium intake was estimated by averaging two 24-h dietary recalls. Cognitive function was evaluated using the Digit Symbol Substitution Test (DSST), which measures processing speed. We applied multivariate logistic regression models to examine the relationship between potassium intake and cognitive function.

Among the 2555 participants included from NHANES 2011-2014, those in the highest quartile of potassium intake (Q4) demonstrated significantly better cognitive function compared to those in the lowest quartile (Q1) (OR = 0.542, 95 % CI: 0.378-0.778, p < 0.05) in the fully adjusted model. The relationship between dietary potassium intake and cognitive function in U.S. adults was found to be nonlinear (p for nonlinear = 0.028). In univariate analysis, as dietary potassium intake increased, the risk of suffering from cognitive decline or abnormalities decreased (OR (Q2) = 0.592; OR (Q3) = 0.401; OR (Q4) = 0.34; p < 0.001). In statistically significant subgroup analyses, it was also found that people with high dietary potassium intake were at less risk of cognitive impairment or abnormalities than those with low dietary potassium intake (p < 0.001).

Higher dietary potassium intake may reduce the risk of cognitive decline or abnormalities in older adults.

Happiness is important to most people in our society, although it is given little importance in political and social objectives. However, happiness is an important topic in various philosophical schools and in Western philosophy, happiness goes back to Aristotelianism and Stoic philosophy. Recent longitudinal studies clearly suggest that happiness depends on interpersonal relationships. So what does otorhinolaryngology have to do with this? In our view, various basic skills that enable people to achieve social fitness, i.e., to establish short- and long-term relationships, are at the center of ENT medicine. Examples of this are hearing, olfaction, the voice, but also facial movements. The multisensory processing of various perception and expression channels creates a "social brain network" as a neuronal correlate of social skills and fitness. Consequently, otorhinolaryngology should play a central role in understanding these abilities in the context of happiness.

Timely clinical diagnosis of Alzheimer's disease and related dementias (ADRD) is important for resource allocation, mitigating safety concerns, and improving quality of life. While studies have examined ADRD diagnosis disparities by race/ethnicity, few include its intersection with nativity. Our aims were to (1) estimate the odds of diagnosed ADRD among US- and foreign-born racial/ethnic groups compared to US-born White older adults and (2) make comparisons by nativity within each racial/ethnic group. We linked 2000-2017 National Health Interview Survey (NHIS) and 2001-2018 Medical Expenditure Panel Survey (MEPS) data (65 + years; n = 38,033). Race/ethnicity and nativity were measured using NHIS data. Diagnosed ADRD was determined using ICD-9 (290/294/331/797) or ICD-10 (F01/F03/G30/G31) billing codes created from self-reports during MEPS household interviews. Bivariate and multivariable analyses were adjusted for covariates based on Anderson's behavioral model of health services use. US-born Black (OR = 1.74; 95% CI = 1.48-2.05), Hispanic (OR = 1.62; 95% CI = 1.14-2.29), and foreign-born Hispanic (OR = 1.63; 95% CI = 1.24-2.15) older adults, but not foreign-born Black or Asian older adults, had higher odds of diagnosed ADRD compared to US-born White older adults after adjusting for age and sex. After additional adjustment for education, health insurance, usual source of care, and chronic conditions, only US-born Black older adults continued to show higher odds (OR = 1.54; 95% CI = 1.27-1.87) of diagnosed ADRD compared to US-born White older adults. There were no differences in ADRD diagnosis by nativity within each racial/ethnic group. Findings highlight the need for including nativity in studies comparing racial/ethnic groups to Whites to fully capture the ADRD burden among US-born Black older adults.

Traumatic brain injuries (TBI) are a considerable health burden on adolescents and young adults. This study aims to assess the influence of health compromising behavior, poor perceived health, poor school success, and low family socioeconomic background during adolescence on subsequent TBI in a large cohort of Finnish adolescents with an average 25-year follow-up.

Baseline Finnish Adolescent Health and Lifestyle survey data gathered biennially (1981-1997) was linked with the diagnosis of subsequent TBI from the Finnish Care Register for Health Care. A structural equation modeling (SEM) was used to analyze the associations between health behavior, poor perceived health, poor school success, and low family socioeconomic background during adolescence on subsequent TBI.

Total of 41 336 persons were included in the analyses. During the follow-up, 1 459 (3.5 %) TBIs occurred. Men were more likely to suffer a TBI. The mean follow-up time was 25.3 years (SD 4.0) and the mean age at the time of TBI was 32.1 years (SD 7.7). Health compromising behavior and not living with both parents in adolescence were associated with the increased risk of TBI. Also, poor perceived health and stress symptoms increased the risk of TBI. Low family socioeconomic status (SES) was only indirectly associated with TBI trough health compromising behavior.

The main finding was that health compromising behavior was associated with TBI, and low family SES was associated with TBI through health compromising behavior in later life. Poor perceived health, stress symptoms, and not living with both parents in adolescence increased the risk of TBI, too. Our findings suggest that adolescents who are at risk of drifting into health compromising behavior and report stress symptoms have an increased risk of TBI in later life.

Low socioeconomic position (SEP) throughout the life course is related to poorer cognitive health in later life, but debate ensues on the life course models for this association. To advance inquiry on the topic, we conducted a scoping review.