Alzheimer's disease (AD) is the most debilitating form of dementia, characterized by amyloid-β (Aβ)-related toxic mechanisms such as oxidative stress, neuroinflammation, and mitochondrial dysfunction. The development of AD is influenced by environmental factors linked to lifestyle, including physical and mental inactivity, diet, and smoking, all of which have been associated with the severity of the disease and Aβ-related pathology. In this study, we used differentiated SH-SY5Y neuroblastoma and C6 glioma cells to investigate the neuroprotective and anti-inflammatory effects of daidzein, a naturally occurring isoflavone, in the context of Aβ oligomer-related toxicity. We observed that pre-treatment with daidzein prevented Aβ-induced cell viability loss, increased oxidative stress, and mitochondrial membrane potential decline in both SH-SY5Y and C6 cells. Furthermore, daidzein application reduced elevated levels of MAPK pathway proteins, pro-inflammatory molecules (cyclooxygenase-2 and IL-1β), and pyroptosis markers, including caspase-1 and gasdermin D, all of which were increased by Aβ exposure. These findings strongly suggest that daidzein alleviates inflammation and toxicity caused by Aβ oligomers. Our results indicate that daidzein could be a potential therapeutic agent for AD and other Aβ-related neurodegenerative diseases.

Alzheimer's disease, a complex and progressive neurological disorder, is the leading cause of late-life dementia. Pathologically, it is marked by the presence of amyloid plaques and neurofibrillary tangles in the brain. Over the past two decades, advancements in understanding the disease's pathogenesis have spurred research into new pharmacological treatments that target its underlying mechanisms. Currently available drugs, such as acetylcholinesterase inhibitors (rivastigmine, galantamine, donepezil) and the NMDA receptor antagonist memantine, primarily address symptoms and are effective only in the later stages of the disease. While these medications can slow disease progression and provide symptomatic relief, they do not offer a cure. Despite having a clear understanding of Alzheimer's neuropathology, the precise mechanisms driving the disease remain elusive. The lack of effective treatments that can stop the start and progression of the disease may be caused by our incomplete understanding of the pathogenic process. New therapeutic targets are now available due to the significant advancements made in pathophysiology over the past few years, which should allow for a direct attack on the underlying illness process. The various pathophysiological pathways that underlie Alzheimer's disease and how it is managed by conventional medication therapy, including current exploratory therapeutic options, are covered in this review article. Innovative, beneficial policies are essential to determine and progress therapeutic molecules to defend against AD.

This primary research paper emphasizes cross-validation, where data samples are reshuffled in each iteration to form randomized subsets divided into n folds. This method improves model performance and achieves higher accuracy than the baseline model. The novelty lies in the data preparation process, where numerical features were imputed using the mean, categorical features were imputed using chi-square methods, and normalization was applied. This research study involves transforming the original datasets and comparative model analysis of four Logistic Regression (LR), Support Vector Machine (SVM), K-Nearest Neighbor (KNN), and Random Forest (RF) cross-validation methodologies to heart disease open datasets. The objective is to easily identify the average accuracy of model predictions and subsequently make recommendations for model selection based on data preprocessing cross-validation model increased (5 to 14%) more than baseline model for best model selection. From comparing each model's accuracy scores, it is found that the logistic regression and k-nearest neighbor models achieved the highest accuracy of 81% among the four models when single accuracy is a concern. However, the random forest model summary statistics attained an F1 score of 95%, precision (96%), and recall (97%), indicating the highest overall macro accuracy score. These findings can be further compared using learning curve validation. Conversely, the logistic regression model exhibited the lowest accuracy of 84% among the four machine learning models. However, this research does not cover hyperparameter optimization, which could potentially improve model performance.

Alzheimer's disease (AD) is a neurodegenerative disorder influenced by both genetic and environmental factors. Identifying therapeutic targets and interventions remains challenging. This study utilized Mendelian Randomization (MR) to investigate causal relationships between plasma proteins, lifestyle factors, and AD, along with virtual screening to identify potential drug compounds. A two-sample MR analysis assessed associations between plasma proteins, identified through genome-wide association studies (GWAS), and AD risk. Co-localization analysis (CA) confirmed the overlap between protein expression and AD susceptibility loci, and reverse MR ruled out reverse causality. A protein-protein interaction (PPI) network was constructed to explore therapeutic targets, followed by virtual screening to identify small-molecule inhibitors for selected proteins. The analysis found significant associations between eight plasma proteins and AD, with five proteins (GSTP1, BIN1, Siglec-3, SERPINF2, and GRN) showing strong evidence of involvement in AD pathogenesis. Virtual screening identified six compounds as potential inhibitors of GSTP1 and four compounds as potential inhibitors of BIN1. Furthermore, MR analysis of lifestyle factors, such as dietary behaviors and smoking cessation, indicated they may influence AD risk through their effects on specific proteins. These findings offer novel insights into the genetic mechanisms underlying AD and highlight the potential of combining MR with virtual screening to identify therapeutic targets. The study also suggests that lifestyle modifications could offer alternative prevention and treatment strategies for AD. Future research should focus on the experimental validation of the identified compounds and further explore the mechanisms linking lifestyle factors to AD.

This study explored how adherence to the DASH diet relates to electrophysiological measures in individuals at varying Alzheimer's disease (AD) risk due to family history (FH). There were 179 dementia-free subjects. DASH index was calculated, and participants were classified into different DASH adherence groups. Tertiles of relative alpha power in default mode network (DMN) regions were calculated. Multivariate logistic regression models were used to examine the association. Lower DASH adherence was associated with decreased odds of higher relative alpha power in the DMN, observed across the entire sample and specifically among those without a FH of AD. Logistic regression models indicated that participants with poorer DASH adherence had a reduced likelihood of elevated DMN alpha power, potentially influenced by vascular and amyloid-beta mechanisms. These findings underscore the dietary pattern's potential role in neural activity modulation, particularly in individuals not genetically predisposed to AD.

Numerous epidemiological studies indicate that populations exposed to environmental toxicants such as heavy metals have a higher likelihood of developing Alzheimer's disease (AD) compared to those unexposed, indicating a potential association between heavy metals exposure and AD. The aim of this review is to summarize contemporary mechanistic research exploring the associations of four important metals, arsenic (As), manganese (Mn), lead (Pb), and cadmium (Cd), with AD and possible pathways, processes, and molecular mechanisms on the basis of data from the most recent mechanistic studies. Primary research publications published during the last decade were identified via a search of the PubMed Database. A thorough literature search and final screening yielded 45 original research articles for this review. Of the 45 research articles, 6 pertain to As, 9 to Mn, 21 to Pb, and 9 to Cd exposures and AD pathobiology. Environmental exposure to these heavy metals induces a wide range of pathological processes that intersect with well-known mechanisms leading to AD, such as oxidative stress, mitochondrial dysfunction, protein aggregation, neuroinflammation, autophagy dysfunction, and tau hyperphosphorylation. While exposure to single metals shares some affected pathways, certain effects are unique to specific metals. For instance, Pb disrupts the blood-brain barrier (BBB) and mitochondrial functions and alters AD-related genes epigenetically. Cd triggers neuronal senescence via p53/p21/Rb. As disrupts nitric oxide (NO) signaling, cortical, and synaptic function. Mn causes glutamate excitotoxicity and dopamine neuron damage. Our review provides a deeper understanding of biological mechanisms showing how metals contribute to AD. Information regarding the potential metal-induced toxicity relevant to AD may help us develop effective therapeutic AD intervention, treatment, and prevention.

Aging is an extremely significant risk associated with neurodegeneration. The most prevalent neurodegenerative disorders (NDs), such as Alzheimer's disease (AD) are distinguished by the prevalence of proteinopathy, aberrant glial cell activation, oxidative stress, neuroinflammation, defective autophagy, cellular senescence, mitochondrial dysfunction, epigenetic changes, neurogenesis suppression, increased blood-brain barrier permeability, and intestinal dysbiosis that is excessive for the patient's age. Substantial body studies have documented a close relationship between gut microbiota and AD, and restoring a healthy gut microbiota may reduce or even ameliorate AD symptoms and progression. Thus, control of the microbiota in the gut has become an innovative model for clinical management of AD, and rising emphasis is focused on finding new techniques for preventing and/or managing the disease. The etiopathogenesis of gut microbiota in driving AD progression and supplementing postbiotics as a preventive and therapeutic treatment for AD is discussed. The review additionally discusses the use of postbiotics in AD prophylaxis and therapy, portraying them as substances that address senescence-triggered dysfunctions and are worthy of translating from bench to biopharmaceutical market in response to "silver consumers" needs. The current review examines and evaluates the impact of postbiotics as whole and specific metabolites, such as short-chain fatty acids (SCFAs), lactate, polyamines, polyphenols, tryptophan metabolites, exopolysaccharides, and bacterial extracellular vesicles, on the aging-associated processes that reinforce AD. Moreover, it provides an overview of the most recent data from both clinical and preclinical research involving the use of postbiotics in AD.

Body composition analysis (BCA) is primarily used in the management of conditions such as obesity and endocrine disorders. However, its potential in providing nutritional guidance for patients with Alzheimer's disease (AD) remains relatively unexplored.

To explore the clinical efficacy of BCA-based dietary nutrition scheme on bone metabolism in AD patients.

This retrospective study included 96 patients with AD complicated by osteoporosis who were admitted to The Third Hospital of Quzhou between January 2023 and December 2024. Based on data from previous similar studies, the patients were randomly assigned to either a routine diet (RD) group (n = 48) or a personalized nutrition (PN) group (n = 48). The RD group received conventional dietary guidance, while the PN group received individualized diet intervention measures based on human BCA. The intervention period lasted for 12 weeks. Bone mineral density (BMD), body mass index (BMI), muscle mass, mineral content, osteocalcin, 25-hydroxyvitamin D, procollagen type I N-terminal propeptide (PINP), beta C-terminal telopeptide of type I collagen (β-CTX), and serum calcium were measured and compared between the two groups before and 12 weeks after the intervention.

No significant differences were observed between groups in terms of age, sex, height, BMI, or other baseline data (P > 0.05). In both groups, BMI did not show significant changes after the intervention (P > 0.05), whereas muscle mass and mineral content were significantly increased (P < 0.05). After the intervention, BMI in the PN group did not differ significantly from that of the RD group, but muscle mass and mineral content were significantly higher in the PN group (P < 0.05). After the intervention, a higher proportion of patients in the PN group had a T score > -1 compared to the RD group (P < 0.05). The mini-mental state examination (MMSE) score was similar in both groups before the intervention. However, 12 weeks after the intervention, the MMSE score in the PN group was significantly higher than that in the RD group (P < 0.05). In both groups, the MMSE score significantly increased 12 weeks post-intervention compared to pre-intervention levels (P < 0.05). Before the intervention, the levels of osteocalcin, serum calcium, PINP, β-CTX, and 25-hydroxyvitamin D were not significantly different between the two groups (P > 0.05). After 12 weeks of intervention, the PN group exhibited higher levels of osteocalcin, serum calcium, and 25-hydroxyvitamin D, as well as lower levels of PINP and β-CTX, compared to the RD group (P < 0.05). In both groups, osteocalcin, serum calcium, and 25-hydroxyvitamin D levels were significantly higher, while PINP and β-CTX levels were significantly lower after 12 weeks of intervention compared to baseline (P < 0.05).

The human BCA-based dietary nutrition regimen plays a crucial role in improving BMD and bone metabolism, with effects that surpass those of conventional nutrition strategies. The findings of this study provide strong evidence for the nutritional management of AD patients.

The comprehensive impact of polysocial risk score (PsRS)-encompassing multiple social determinants of health (SDoHs) with genetic and lifestyle factors on dementia incidence remains to be elucidated.

This study aimed to clear the associations between PsRS and dementia incidence and evaluated how genetic and lifestyle factors modified these associations in the UK Biobank cohort.

The detailed prospective study involved over 500,000 participants when recruited in 2006-2010. The PsRS was calculated by 12 SDoHs across psychosocial factors, socioeconomic status, and neighborhood and living environment. A healthy lifestyle score was constructed from physical activities, alcohol consumption, smoking status, and diet. A genetic risk score (GRS) was computed via genotype data from UK Biobank. The Cox proportional hazards model was used to estimate hazard ratios (HRs) and 95 % confidence intervals (CIs) for the association between PsRS, lifestyle factors, GRS and dementia.

Results showed the participants with intermediate (HR = 1.32, 95%CI: 1.20-1.45) and high PsRS (HR = 2.10, 95 % CI: 1.91-2.32) were significantly associated with an increased risk of dementia compared with those with a low PsRS. Then, compared with participants with low PsRS and favorable lifestyle/low GRS, high PsRS and unfavorable lifestyle/high GRS had the highest risk of dementia (HR = 3.11,95%CI: 2.63-3.68)/(HR = 3.56, 95%CI: 2.62-4.85).

Both high PsRS and GRS were significantly associated with higher dementia risk. A favorable lifestyle could reduce dementia incidence regardless of high PsRS or GRS. Additionally, focusing on the intervention of SDoHs would be positive in preventing dementia.

Alzheimer's disease (AD) is a major neurodegenerative dementia, with its complex pathophysiology challenging current treatments. Recent advancements have shifted the focus from the traditionally dominant amyloid hypothesis toward a multifactorial understanding of the disease. Emerging evidence suggests that while amyloid-beta (Aβ) accumulation is central to AD, it may not be the primary driver but rather part of a broader pathogenic process. Novel hypotheses have been proposed, including the role of tau protein abnormalities, mitochondrial dysfunction, and chronic neuroinflammation. Additionally, the gut-brain axis and epigenetic modifications have gained attention as potential contributors to AD progression. The limitations of existing therapies underscore the need for innovative strategies. This study explores the integration of machine learning (ML) in drug discovery to accelerate the identification of novel targets and drug candidates. ML offers the ability to navigate AD's complexity, enabling rapid analysis of extensive datasets and optimizing clinical trial design. The synergy between these themes presents a promising future for more effective AD treatments.

The hippocampus, noted as (HC), plays a crucial role in the processes of learning, memory formation, and spatial navigation. Recent research reveals that this brain region can undergo structural and functional changes due to environmental exposures, including stress, noise pollution, sleep deprivation, and microgravity. This review synthesizes findings from animal and human studies, emphasizing the HC's plasticity in response to these factors. It examines changes in volume, architecture, neurogenesis, synaptic plasticity, and gene expression and highlights critical periods of vulnerability to environmental influences impacting cognition and behavior. It also investigates underlying mechanisms such as glucocorticoid signaling, epigenetic alterations, and neural circuit adaptations. Understanding how the HC reacts to various environmental exposures is vital for developing strategies to enhance cognitive resilience and mitigate negative effects on this crucial brain region. Further research is needed to identify protective and risk factors and create effective interventions.

Alzheimer's disease (AD) is a chronic, progressive neurodegenerative disorder characterized by cognitive decline, memory loss, and impaired reasoning. It is the leading cause of dementia in older adults, marked by the pathological accumulation of amyloid-beta plaques and neurofibrillary tangles. These pathological changes lead to widespread neuronal damage, significantly impacting daily functioning and quality of life.

This comprehensive review aims to explore various aspects of Alzheimer's disease, including its epidemiology, risk factors, clinical presentation, diagnostic advancements, management strategies, caregiving challenges, and emerging therapeutic interventions.

A systematic literature review was conducted across multiple electronic databases, including PubMed, MEDLINE, Cochrane Library, and Scopus, from their inception to May 2024. The search strategy incorporated a combination of keywords and Medical Subject Headings (MeSH) terms such as "Alzheimer's disease," "epidemiology," "risk factors," "symptoms," "diagnosis," "management," "caregiving," "treatment," and "novel therapies." Boolean operators (AND, OR) were used to refine the search, ensuring a comprehensive analysis of the existing literature on Alzheimer's disease.

AD is significantly influenced by genetic predispositions, such as the apolipoprotein E (APOE) ε4 allele, along with modifiable environmental factors like diet, physical activity, and cognitive engagement. Diagnostic approaches have evolved with advances in neuroimaging techniques (MRI, PET), and biomarker analysis, allowing for earlier detection and intervention. The National Institute on Aging and the Alzheimer's Association have updated diagnostic criteria to include biomarker data, enhancing early diagnosis.

The management of AD includes pharmacological treatments, such as cholinesterase inhibitors and NMDA receptor antagonists, which provide symptomatic relief but do not slow disease progression. Emerging therapies, including amyloid-beta and tau-targeting treatments, gene therapy, and immunotherapy, offer potential for disease modification. The critical role of caregivers is underscored, as they face considerable emotional, physical, and financial burdens. Support programs, communication strategies, and educational interventions are essential for improving caregiving outcomes. While significant advancements have been made in understanding and managing AD, ongoing research is necessary to identify new therapeutic targets and enhance diagnostic and treatment strategies. A holistic approach, integrating clinical, genetic, and environmental factors, is essential for addressing the multifaceted challenges of Alzheimer's disease and improving outcomes for both patients and caregivers.

One of the important markers affecting aging processes is the increase in inflammatory markers. Many chronic diseases are associated with inflammation and chronic inflammation increases with aging. Inflammation can change with dietary components. Foods, compounds and nutrients that have anti-inflammatory or proinflammatory properties attract attention. According to the Dietary Inflammatory Index, positive scores are obtained if the nutrient has a proinflammatory effect on cytokines, and negative scores are obtained if it has an anti-inflammatory effect.

A higher proinflammatory diet is associated with cardiometabolic diseases, neurodegenerative disease, cancers and musculoskeletal health and related mortality. In this study, its relationship with type 2 diabetes mellitus, obesity, metabolic syndrome, musculoskeletal diseases, dementia, depression and cancer, which are more common in older adults and known to be associated with inflammation, was examined. Although studies involving under 65 years old are more prevalent, research involving older adults and Dietary Inflammatory Index (DII) is more limited. It is known that chronic inflammation increases with aging. Diet is one of the factors affecting inflammation. In the light of these investigations, the topics of anti-inflammatory nutrition and DII for the treatment of inflammation-related diseases in older adults are strong and open to development topics of discussion. Despite the significant interest in the potential positive effects of anti-inflammatory nutrition on diseases, contributing to clearer evidence of its protective effects on health necessitates further randomized controlled trials, in vivo, in vitro, cell, animal, human and case-control studies for better risk assessment.

Substantial sleep impairment in patients with Alzheimer's disease (AD) is one of the emerging points for continued efforts to better understand the disease. Individuals without cognitive decline, an important marker of the clinical phase of AD, may show early alterations in the sleep-wake cycle. The objective of this critical narrative review is to explore the bidirectional pathophysiological correlation between sleep disturbances and Alzheimer's Disease. Specifically, it examines how the disruption of sleep homeostasis in individuals without dementia could contribute to the pathogenesis of AD, and conversely, how neurodegeneration in individuals with Alzheimer's Disease might lead to dysregulation of the sleep-wake cycle. Recent scientific results indicate that sleep disturbances, particularly those related to impaired glymphatic clearance, may act as an important mechanism associated with the genesis of Alzheimer's Disease. Additionally, amyloid deposition and tau protein hyperphosphorylation, along with astrocytic hyperactivation, appear to trigger changes in neurotransmission dynamics in areas related to sleep, which may explain the onset of sleep disturbances in individuals with AD. Disruption of sleep homeostasis appears to be a modifiable risk factor in Alzheimer's disease. Whenever possible, the use of non-pharmacological strategies becomes important in this context. From a different perspective, additional research is needed to understand and treat the dysfunction of the sleep-wake cycle in individuals already affected by AD. Early recognition and correction of sleep disturbances in this population could potentially mitigate the progression of dementia and improve the quality of life for those with AD.

Recent studies underscore the role of gut and oral microbiota in influencing neuroinflammation through the microbiota-gut-brain axis, including in Alzheimer's disease (AD). This review aims to provide a comprehensive synthesis of recent findings on the involvement of gut and oral microbiota in the neuroinflammatory processes associated with AD, emphasizing novel insights and therapeutic implications. This review reveals that dysbiosis in AD patients' gut and oral microbiota is linked to heightened peripheral and central inflammatory responses. Specific bacterial taxa, such as Bacteroides and Firmicutes in the gut, as well as Porphyromonas gingivalis in the oral cavity, are notably altered in AD, leading to significant changes in microglial activation and cytokine production. Gut microbiota alterations are associated with increased intestinal permeability, facilitating the translocation of endotoxins like lipopolysaccharides (LPS) into the bloodstream and exacerbating neuroinflammation by activating the brain's toll-like receptor 4 (TLR4) pathways. Furthermore, microbiota-derived metabolites, including short-chain fatty acids (SCFAs) and amyloid peptides, can cross the blood-brain barrier and modulate neuroinflammatory responses. While microbial amyloids may contribute to amyloid-beta aggregation in the brain, certain SCFAs like butyrate exhibit anti-inflammatory properties, suggesting a potential therapeutic avenue to mitigate neuroinflammation. This review not only highlights the critical role of microbiota in AD pathology but also offers a ray of hope by suggesting that modulating gut and oral microbiota could represent a novel therapeutic strategy for reducing neuroinflammation and slowing disease progression.

Cognitive impairment is projected to affect a preponderant proportion of the aging population. Lifelong dietary habits have been hypothesized to play a role in preventing cognitive decline. Among the most studied dietary components, fish consumptionhas been extensively studied for its potential effects on the human brain.

To perform a meta-analysis of observational studies exploring the association between fish intake and cognitive impairment/decline and all types of dementia.

A systematic search of electronic databases was performed to identify observational studies providing quantitative data on fish consumption and outcomes of interest. Random effects models for meta-analyses using only extreme exposure categories, subgroup analyses, and dose-response analyses were performed to estimate cumulative risk ratios (RRs) and 95% confidence intervals (CIs).

The meta-analysis comprised 35 studies. Individuals reporting the highest vs. the lowest fish consumption were associated with a lower likelihood of cognitive impairment/decline (RR = 0.82, 95% CI: 0.75, 0.90, I2 = 61.1%), dementia (RR = 0.82, 95% CI: 0.73, 0.93, I2 = 38.7%), and Alzheimer's disease (RR = 0.80, 95% CI: 0.67, 0.96, I2 = 20.3%). The dose-response relation revealed a significantly decreased risk of cognitive impairment/decline and all cognitive outcomes across higher levels of fish intake up to 30% for 150 g/d (RR = 0.70, 95% CI: 0.52, 0.95). The results of this relation based on APOE ε4 allele status was mixed based on the outcome investigated.

Current findings suggest fish consumption is associated with a lower risk of cognitive impairment/decline in a dose-response manner, while for dementia and Alzheimer's disease there is a need for further studies to improve the strength of evidence.

This narrative review evaluates the role of diet in the relationship between depression and Alzheimer's disease (AD).

AD and depression are often comorbid, and depression appears to independently increase the future risk of AD. Evidence suggests diet influences the risk of both conditions directly and indirectly. Diet impacts neurochemical and biological processes that may affect the development and progression of depression and cognitive dysfunction. The dietary components offering the greatest protection against depression and AD are yet to be determined. Current evidence highlights the importance of polyphenolic compounds, folate, B vitamins, and polyunsaturated fatty acids, along with adherence to dietary patterns like the Mediterranean diet, which includes multiple beneficial dietary factors.

The investigation of dietary factors in the prevention of depression and AD is a comparatively young field of research. Comprehensive highly characterised longitudinal datasets and advanced analytical approaches are required to further examine the complex relationship between diet, depression, and AD. There is a critical need for more research in this area to develop effective preventive strategies aimed at maintaining mental and physical health with advancing age.

The rhizomes of Acorus tatarinowii Schott and Acorus gramineus Solander are widely used for treating amnesia in traditional Chinese medicine. In contrast, their leaves are usually discarded without their medicinal properties being known. Here, we found that the hot water extract of leaves improved cognition and tau pathology in model mice of frontotemporal dementia, similar to or even better than that of rhizomes. To explore the optimal method of processing, we made three preparations from dried leaves: hot water extract, extraction residue, and non-extracted simple crush powder. Among them, the simple crush powder had the strongest effect on tauopathy in mice. The crush powder also ameliorated Aβ and α-synuclein pathologies and restored cognition in mouse models of Alzheimer's disease and dementia with Lewy bodies. These findings suggest the potential of Acorus tatarinowii/gramineus leaves as a dietary source for dementia prevention and reveal that simple crushing is a better way to maximize their efficacy.

Epigenetics defines changes in cell function without involving alterations in DNA sequence. Neuroepigenetics bridges neuroscience and epigenetics by regulating gene expression in the nervous system and its impact on brain function. With the increase in research in recent years, it was observed that alterations in the gene expression did not always originate from changes in the genetic sequence, which has led to understanding the role of epigenetics in neurodegenerative diseases (NDDs) including Alzheimer's disease (AD) and Parkinson's disease (PD). Epigenetic alterations contribute to the aberrant expression of genes involved in neuroinflammation, protein aggregation, and neuronal death. Natural phytochemicals have shown promise as potential therapeutic agents against NDDs because of their antioxidant, anti-inflammatory, and neuroprotective effects in cellular and animal models. For instance, resveratrol (grapes), curcumin (turmeric), and epigallocatechin gallate (EGCG; green tea) exhibit neuroprotective effects through their influence on DNA methylation patterns, histone acetylation, and non-coding RNA expression profiles. Phytochemicals also aid in slowing disease progression, preserving neuronal function, and enhancing cognitive and motor abilities. The present review focuses on various epigenetic modifications involved in the pathology of NDDs, including AD and PD, gene expression regulation related to epigenetic alterations, and the role of specific polyphenols in influencing epigenetic modifications in AD and PD.

Prior observational research has investigated the association between dietary patterns and Alzheimer's disease (AD) risk. Nevertheless, due to constraints in past observational studies, establishing a causal link between dietary habits and AD remains challenging.

Methodology involved the utilization of extensive cohorts sourced from publicly accessible genome-wide association study (GWAS) datasets of European descent for conducting Mendelian randomization (MR) analyses. The principal analytical technique utilized was the inverse-variance weighted (IVW) method.

The MR analysis conducted in this study found no statistically significant causal association between 20 dietary habits and the risk of AD (All p > 0.05). These results were consistent across various MR methods employed, including MR-Egger, weighted median, simple mode, and weighted mode approaches. Moreover, there was no evidence of horizontal pleiotropy detected (All p > 0.05).

In this MR analysis, our finding did not provide evidence to support the causal genetic relationships between dietary habits and AD risk.

This comprehensive review explores the dynamic relationship between sports, nutrition, and neurological health. Focusing on recent clinical advancements, it examines how physical activity and dietary practices influence the prevention, treatment, and rehabilitation of various neurological conditions. The review highlights the role of neuroimaging in understanding these interactions, discusses emerging technologies in neurotherapeutic interventions, and evaluates the efficacy of sports and nutritional strategies in enhancing neurological recovery. This synthesis of current knowledge aims to provide a deeper understanding of how lifestyle factors can be integrated into clinical practices to improve neurological outcomes.

Resveratrol (RV), a natural compound found in grapes, berries, and peanuts, has been extensively studied for its potential in treating Alzheimer's disease (AD). RV has shown promise in inhibiting the formation of beta-amyloid plaques (Aβ) and neurofibrillary tangles (NFTs), protecting against neuronal damage and oxidative stress, reducing inflammation, promoting neuroprotection, and improving the function of the blood-brain barrier (BBB). However, conflicting results have been reported, necessitating a comprehensive umbrella review of systematic reviews to provide an unbiased conclusion on the therapeutic effectiveness of RV in AD.

The objective of this study was to systematically synthesize and evaluate systematic and meta-analysis reviews investigating the role of RV in AD using data from both human and animal studies.

Of the 34 systematic and meta-analysis reviews examining the association between RV and AD that were collected, six were included in this study based on specific selection criteria. To identify pertinent studies, a comprehensive search was conducted in English-language peer-reviewed journals without any restrictions on the publication date until October 15, 2023. The search was carried out across multiple databases, including Embase, MEDLINE (PubMed), Cochrane Library, Web of Science, and Google Scholar, utilizing appropriate terms relevant to the specific research field. The AMSTAR-2 and ROBIS tools were also used to evaluate the quality and risk of bias of the included systematic reviews, respectively. Two researchers independently extracted and analyzed the data, resolving any discrepancies through consensus. Of note, the study adhered to the PRIOR checklist.

This umbrella review presented robust evidence supporting the positive impacts of RV in AD, irrespective of the specific mechanisms involved. It indeed indicated that all six systematic and meta-analysis reviews unanimously concluded that the consumption of RV can be effective in the treatment of AD.

RV exhibits promising potential for benefiting individuals with AD through various mechanisms. It has been observed to enhance cognitive function, reduce Aβ accumulation, provide neuroprotection, protect the BBB, support mitochondrial function, facilitate synaptic plasticity, stabilize tau proteins, mitigate oxidative stress, and reduce neuroinflammation commonly associated with AD.

Alzheimer's disease (AD) is a major global health problem today and is the most common form of dementia. AD is characterized by the formation of β-amyloid (Aβ) plaques and neurofibrillary clusters, leading to decreased brain acetylcholine levels in the brain. Another mechanism underlying the pathogenesis of AD is the abnormal phosphorylation of tau protein that accumulates at the level of neurofibrillary aggregates, and the areas most affected by this pathological process are usually the cholinergic neurons in cortical, subcortical, and hippocampal areas. These effects result in decreased cognitive function, brain atrophy, and neuronal death. Malnutrition and weight loss are the most frequent manifestations of AD, and these are also associated with greater cognitive decline. Several studies have confirmed that a balanced low-calorie diet and proper nutritional intake may be considered important factors in counteracting or slowing the progression of AD, whereas a high-fat or hypercholesterolemic diet predisposes to an increased risk of developing AD. Especially, fruits, vegetables, antioxidants, vitamins, polyunsaturated fatty acids, and micronutrients supplementation exert positive effects on aging-related changes in the brain due to their antioxidant, anti-inflammatory, and radical scavenging properties. The purpose of this review is to summarize some possible nutritional factors that may contribute to the progression or prevention of AD, understand the role that nutrition plays in the formation of Aβ plaques typical of this neurodegenerative disease, to identify some potential therapeutic strategies that may involve some natural compounds, in delaying the progression of the disease.

Dementia is one of the most significant global challenges in medical and social care in the 21st century. It affects not only the patients themselves, but also their families, caregivers, and society in general, causing physical, psychological, and socioeconomic effects. As of 2020, there are approximately 6 million people in Japan aged 65 or older with dementia, and this number is expected to increase to around 7 million by 2025, meaning that one out of every five elderly people will have dementia. To prevent the onset and progression of dementia, it is crucial to have a proper understanding of its risks and adopt a healthy lifestyle. Leading an active life from an early stage can also aid in delaying or preventing the onset of dementia. Livingston has identified 12 risks that can lead to dementia, including physical inactivity, smoking, excessive alcohol consumption, air pollution, head injury, social isolation, poor educational history, obesity, hypertension, diabetes, depression, and hearing loss. Modifying one's lifestyle and leading an active life can be crucial in reducing these risks. The Mediterranean diet is gaining attention as a good practice for dementia prevention due to its diversity, richness in omega-3 fatty acids and vitamins. Exercise has been shown to prevent dementia on biological, behavioral, and socio-psychological levels. Repetitive transcranial magnetic stimulation is a non-invasive brain stimulation method that can alter brain plasticity and is being studied for clinical applications as a non-drug therapy for preventing dementia progression.

The advent of high-throughput 'omics' technologies has improved our knowledge of gut microbiome in human health and disease, including Alzheimer's disease (AD), a neurodegenerative disorder. Frequent bidirectional communications and mutual regulation exist between the gastrointestinal tract and the central nervous system through the gut-brain axis. A large body of research has reported a close association between the gut microbiota and AD development, and restoring a healthy gut microbiota may curb or even improve AD symptoms and progression. Thus, modulation of the gut microbiota has become a novel paradigm for clinical management of AD, and emerging effort has focused on developing potential novel strategies for preventing and/or treating the disease. In this review, we provide an overview of the connection and causal relationship between gut dysbiosis and AD, the mechanisms of gut microbiota in driving AD progression, and the successes and challenges of implementing available gut microbiome-targeted therapies (including probiotics, prebiotics, synbiotics, postbiotics, and fecal microbiota transplantation) in preventive and/or therapeutic preclinical and clinical intervention studies of AD. Finally, we discuss the future directions in this field.

One of the most complex and challenging developments at the beginning of the third millennium is the alarming increase in demographic aging, mainly-but not exclusively-affecting developed countries. This reality results in one of the harsh medical, social, and economic consequences: the continuously increasing number of people with dementia, including Alzheimer's disease (AD), which accounts for up to 80% of all such types of pathology. Its large and progressive disabling potential, which eventually leads to death, therefore represents an important public health matter, especially because there is no known cure for this disease. Consequently, periodic reappraisals of different therapeutic possibilities are necessary. For this purpose, we conducted this systematic literature review investigating nonpharmacological interventions for AD, including their currently known cellular and molecular action bases. This endeavor was based on the PRISMA method, by which we selected 116 eligible articles published during the last year. Because of the unfortunate lack of effective treatments for AD, it is necessary to enhance efforts toward identifying and improving various therapeutic and rehabilitative approaches, as well as related prophylactic measures.