Dementia In Elderly Population Research Articles

Physical Exercise Counteracts Aging-Associated White Matter Demyelination Causing Cognitive Decline.

In the central nervous system, oligodendrocytes wrap around neuronal axons to form myelin, an insulating layer or sheath that allows for the efficient conductance of action potentials. In addition to structural insulation, myelin provides encased axons with nutrient, metabolic and defensive support. Demyelination, or myelin loss, can therefore cause axonal dysfunction, leading to neurological impairment and disease. In Alzheimer's disease (AD), progressive white matter demyelination is acknowledged as one of the earliest pathologies preceding symptom onset. Unfortunately, current pharmacotherapy for slowing demyelination or promoting remyelination in AD is nonexistent. Exercise is recognized for its wide-ranging benefits to human health, including improved mental health and the prevention of lifestyle-related diseases. Mounting evidence suggests the contribution of physical activity in delaying the progression of dementia in elderly populations. Recent mechanistic studies have shown that exercise facilitates myelination in the brain through the vitalization of intrinsic pro-myelination cues, such as increased neurotrophic factors and electrical activity. In this review, we summarize and discuss the potential of physical exercise on counteracting aging-associated white matter demyelination, which causes cognitive decline in AD. We highlight the need of further basic and clinical research investigations on this topic to establish novel approaches for healthy and improved brain aging.

Exploring the Genetic Predisposition to Epigenetic Changes in Alzheimer's Disease.

Alzheimer's disease (AD) is a prevalent type of dementia in elderly populations with a significant genetic component. The accumulating evidence suggests that AD involves a reconfiguration of the epigenetic landscape, including DNA methylation, post-translational modification of histone proteins, and chromatin remodeling. Along with environmental factors, individual specific genetic features play a considerable role in the formation of epigenetic architecture. In this study, we attempt to identify the non-coding regulatory SNPs (rSNPs) able to affect the epigenetic mechanisms in AD. To this end, the multi-omics approach is used. The GEO (Gene Expression Omnibus) available data (GSE153875) for AD patients and controls are integrated to reveal the rSNPs that display allele-specific features in both ChIP-seq profiles of four histone modifications and RNA-seq. Furthermore, we analyze the presence of rSNPs in the promoters of genes reported to be differentially expressed between AD and the normal brain (AD-related genes) and involved in epigenetic regulation according to the EpiFactors database. We also searched for the rSNPs in the promoters of the genes coding for transcription regulators of the identified AD-related genes. These regulators were selected based on the corresponding ChIP-seq peaks (ENCODE) in the promoter regions of these genes. Finally, we formed a panel of rSNPs localized to the promoters of genes that contribute to the epigenetic landscape in AD and, thus, to the genetic predisposition for this disease.

Whole-body vibration ameliorates glial pathological changes in the hippocampus of hAPP transgenic mice, but does not affect plaque load

BackgroundAlzheimer’s disease (AD) is the core cause of dementia in elderly populations. One of the main hallmarks of AD is extracellular amyloid beta (Aβ) accumulation (APP-pathology) associated with glial-mediated neuroinflammation. Whole-Body Vibration (WBV) is a passive form of exercise, but its effects on AD pathology are still unknown.MethodsFive months old male J20 mice (n = 26) and their wild type (WT) littermates (n = 24) were used to investigate the effect of WBV on amyloid pathology and the healthy brain. Both J20 and WT mice underwent WBV on a vibration platform or pseudo vibration treatment. The vibration intervention consisted of 2 WBV sessions of 10 min per day, five days per week for five consecutive weeks. After five weeks of WBV, the balance beam test was used to assess motor performance. Brain tissue was collected to quantify Aβ deposition and immunomarkers of astrocytes and microglia.ResultsJ20 mice have a limited number of plaques at this relatively young age. Amyloid plaque load was not affected by WBV. Microglia activation based on IBA1-immunostaining was significantly increased in the J20 animals compared to the WT littermates, whereas CD68 expression was not significantly altered. WBV treatment was effective to ameliorate microglia activation based on morphology in both J20 and WT animals in the Dentate Gyrus, but not so in the other subregions. Furthermore, GFAP expression based on coverage was reduced in J20 pseudo-treated mice compared to the WT littermates and it was significantly reserved in the J20 WBV vs. pseudo-treated animals. Further, only for the WT animals a tendency of improved motor performance was observed in the WBV group compared to the pseudo vibration group.ConclusionIn accordance with the literature, we detected an early plaque load, reduced GFAP expression and increased microglia activity in J20 mice at the age of ~ 6 months. Our findings indicate that WBV has beneficial effects on the early progression of brain pathology. WBV restored, above all, the morphology of GFAP positive astrocytes to the WT level that could be considered the non-pathological and hence “healthy” level. Next experiments need to be performed to determine whether WBV is also affective in J20 mice of older age or other AD mouse models.

Pathophysiology, cellular and molecular mechanisms of large and small vessel diseases.

Cerebrovascular disease (CVD) is the second most common cause of cognitive impairment and dementia in aged population. CVD presents in a myriad number of clinical ways based on the functional location of pathology. While primary clinical emphasis has been placed on motor, speech and visual deficits, vascular cognitive decline is a vastly under recognized and devastating condition afflicting millions of Americans. CVD, a disease of the blood vessels that supply blood to brain involves an integration between small and large vessels. Cerebral large vessel diseases (LVD) are associated with atherosclerosis, artery-to-artery embolism, intracardiac embolism and a large vessel stroke leading to substantial functional disability. Cerebral small vessel disease (SVD) is critically involved in stroke, brain hemorrhages, cognitive decline and functional loss in elderly patients. An evolving understanding of cellular and molecular mechanisms emphasizes that inflammatory vascular changes contribute to systemic pathologic conditions of the central nervous systems (CNS), with specific clinical presentations including, cognitive decline. Advances in an understanding of pathophysiology of disease processes and therapeutic interventions may help improve outcomes. This review will focus on large and small vessels diseases and their relationship to vascular cognitive decline, atherosclerosis, stroke, and inflammatory neurodegeneration. We will also emphasize the molecular and cellular mechanisms, as well as genetic and epigenetic factors associated with LVD and SVD.

Identification and validation of oxidative stress and immune-related hub genes in Alzheimer’s disease through bioinformatics analysis

Alzheimer’s disease (AD) is the leading cause of dementia in aged population. Oxidative stress and neuroinflammation play important roles in the pathogenesis of AD. Investigation of hub genes for the development of potential therapeutic targets and candidate biomarkers is warranted. The differentially expressed genes (DEGs) in AD were screened in GSE48350 dataset. The differentially expressed oxidative stress genes (DEOSGs) were analyzed by intersection of DEGs and oxidative stress-related genes. The immune-related DEOSGs and hub genes were identified by weighted gene co-expression network analysis (WGCNA) and protein–protein interaction (PPI) analysis, respectively. Enrichment analysis was performed by Gene Ontology and Kyoto Encyclopedia of Genes and Genomes. The diagnostic value of hub genes was assessed by receiver operating characteristic analysis and validated in GSE1297. The mRNA expression of diagnostic genes was determined by qRT-PCR analysis. Finally, we constructed the drug, transcription factors (TFs), and microRNA network of the diagnostic genes. A total of 1160 DEGs (259 up-regulated and 901 down-regulated) were screened in GSE48350. Among them 111 DEOSGs were identified in AD. Thereafter, we identified significant difference of infiltrated immune cells (effector memory CD8 T cell, activated B cell, memory B cell, natural killer cell, CD56 bright natural killer cell, natural killer T cell, plasmacytoid dendritic cell, and neutrophil) between AD and control samples. 27 gene modules were obtained through WGCNA and turquoise module was the most relevant module. We obtained 66 immune-related DEOSGs by intersecting turquoise module with the DEOSGs and identified 15 hub genes through PPI analysis. Among them, 9 hub genes (CCK, CNR1, GAD1, GAP43, NEFL, NPY, PENK, SST, and TAC1) were identified with good diagnostic values and verified in GSE1297. qRT-PCR analysis revealed the downregulation of SST, NPY, GAP43, CCK, and PENK and upregulation of NEFL in AD. Finally, we identified 76 therapeutic agents, 152 miRNAs targets, and 91 TFs regulatory networks. Our study identified 9 key genes associated with oxidative stress and immune reaction in AD pathogenesis. The findings may help to provide promising candidate biomarkers and therapeutic targets for AD.

Brain CT can predict low lean mass in the elderly with cognitive impairment: a community-dwelling study

BackgroundThe coexistence of sarcopenia and dementia in aging populations is not uncommon, and they may share common risk factors and pathophysiological pathways. This study aimed to evaluate the relationship between brain atrophy and low lean mass in the elderly with impaired cognitive function.MethodsThis cross-sectional study included 168 elderly patients who visited the multi-disciplinary dementia outpatient clinic at Kaohsiung Chang Gung Memorial Hospital for memory issues, between 2017 and 2019. The body composition was assessed by dual energy X-ray absorptiometry (DEXA) and CT based skeletal muscle index including L3 skeletal muscle index (L3SMI) and masseter muscle mass index (MSMI). The brain atrophy assessment was measured by CT based visual rating scale. Possible predictors of low lean mass in the elderly with cognitive impairement were identified by binary logistic regression. ROC curves were generated from binary logistic regression.ResultsAmong the 81 participants, 43 (53%) remained at a normal appendicular skeletal muscle index (ASMI), whereas 38 (47%) showed low ASMI. Compared with the normal ASMI group, subjects with low ASMI exhibited significantly lower BMI, L3SMI, and MSMI (all p < 0.05), and showed significant brain atrophy as assessed by visual rating scale (p < 0.001). The accuracy of predictive models for low ASMI in the elderly with cognitive impairment were 0.875, (Area under curve (AUC) = 0.926, 95% confidence interval [CI] 0.844–0.972) in model 1 (combination of BMI, GCA and L3SMI) and 0.885, (Area under curve (AUC) = 0.931, [CI] 0.857–0.979) in model 2 (combination of BMI, GCA and MSMI).ConclusionsGlobal cortical atrophy and body mass index combined with either L3 skeletal muscle index or masseter skeletal muscle index can predict low lean mass in the elderly with cognitive impairment.

Modulation of Neurolipid Signaling and Specific Lipid Species in the Triple Transgenic Mouse Model of Alzheimer's Disease.

Alzheimer’s disease (AD) is a progressive neurodegenerative disorder and the most common cause of dementia in aging populations. Recently, the regulation of neurolipid-mediated signaling and cerebral lipid species was shown in AD patients. The triple transgenic mouse model (3xTg-AD), harboring βAPPSwe, PS1M146V, and tauP301L transgenes, mimics many critical aspects of AD neuropathology and progressively develops neuropathological markers. Thus, in the present study, 3xTg-AD mice have been used to test the involvement of the neurolipid-based signaling by endocannabinoids (eCB), lysophosphatidic acid (LPA), and sphingosine 1-phosphate (S1P) in relation to the lipid deregulation. [35S]GTPγS autoradiography was used in the presence of specific agonists WIN55,212-2, LPA and CYM5442, to measure the activity mediated by CB1, LPA1, and S1P1 Gi/0 coupled receptors, respectively. Consecutive slides were used to analyze the relative intensities of multiple lipid species by MALDI Mass spectrometry imaging (MSI) with microscopic anatomical resolution. The quantitative analysis of the astrocyte population was performed by immunohistochemistry. CB1 receptor activity was decreased in the amygdala and motor cortex of 3xTg-AD mice, but LPA1 activity was increased in the corpus callosum, motor cortex, hippocampal CA1 area, and striatum. Conversely, S1P1 activity was reduced in hippocampal areas. Moreover, the observed modifications on PC, PA, SM, and PI intensities in different brain areas depend on their fatty acid composition, including decrease of polyunsaturated fatty acid (PUFA) phospholipids and increase of species containing saturated fatty acids (SFA). The regulation of some lipid species in specific brain regions together with the modulation of the eCB, LPA, and S1P signaling in 3xTg-AD mice indicate a neuroprotective adaptation to improve neurotransmission, relieve the myelination dysfunction, and to attenuate astrocyte-mediated neuroinflammation. These results could contribute to identify new therapeutic strategies based on the regulation of the lipid signaling in familial AD patients.

Mitochondrial Dysfunction in Alzheimer’s Disease and Possible Therapeutic Targets to Prevent Progression of Alzheimer’s Disease

Alzheimer’s Disease (AD) is the most frequent cause of dementia in aged population. Till now, there is no effective treatment for AD. Now various studies have kinked AD to mitochondrial dysfunction, due to accumulation of Aβaggregates, neurofibrillary tangles, cholinergic transmission, oxidative stress and neuroinflammation causing neurodegeneration and cognitive decline seen in AD. Here in this article, how the mitochondrial dysfunction/dynamics are involved in the pathogenesis of cognitive decline seen in cases of AD and various therapeutics targeted against mitochondrial dysfunctions are described, thereby causing a ray of hope for preventing progression of AD.

Expanding role of nurses in management of dementia in geriatrics: improving well-being of geriatric patients through quality nursing care

ABSTRACT The potential nurses role to include the recognition and management of dementia has been acknowledged. Practice Nurses are well-positioned to provide comprehensive dementia information and support so that people living with dementia are better equipped to self-manage their health and live well with dementia. However, treatment of geriatric dementia has become difficult owing to co-morbidities and cognitive and physical deterioration of these patients. Thus, geriatric dementia patients require special attention during care in homes and clinical settings. In modern medical practice, the role of nurse has become dynamic, ranging from education and personal care. The profession of nursing is considered as critical to meets the needs of the elderly population with dementia and ensure the delivery of high-quality care. Since nurses play such an important role in caring for these individuals, comprehensive reviews lack on their role and experience in geriatric dementia treatment and issues. This review summarizes the expanding role of nurses in the management of geriatric dementia in terms of nurse’s knowledge, role, communication, attitude and maintaining patient’s quality of life through diverse activities. Furthermore, we also explain the future direction for improving the nursing care to treat dementia in elderly population.

A Review of the Application of Hyperbaric Oxygen Therapy in Alzheimer's Disease.

Alzheimer's disease (AD) is considered as the most common cause of dementia in elderly population. While the exact mechanism of AD has not been discovered, hyperbolic oxygen therapy (HBOT) has been proven to be effective in the treatment of this degenerative disease. The objectives of this article are to review the literature available on molecular and physiological mechanisms underlying HBOT and its efficacy in treating AD and to review the effectiveness of HBOT as an alternate treatment intervention in both human and animal models. 391 full text articles were included in the review after literature search between 1980-2021 from two online data base (ScienceDirect and PubMed). The following key words were used: 'hyperbaric oxygen therapy' and 'Alzheimer disease.' Based on the outcomes of clinical and experimental studies, this review advocates the use of HBOT for the treatment of AD. This review explores future directions and recommends further research into a treatment protocol that will maintain long-term cognitive health of AD patients.

Long-term exposure to ambient air pollution and risk of dementia: Results of the prospective Three-City Study

BackgroundEmerging epidemiological evidence suggests a relationship between exposure to air pollution and dementia. However, most of the existing studies relied on health administrative databases for the diagnosis of dementia. In a large French population-based cohort (the 3C Study), we assessed the effects of particulate matter ≤2.5 µm (PM2.5), nitrogen dioxide (NO2) and black carbon (BC) on the risk of dementia diagnosed with reliable tools. MethodsParticipants aged ≥65 years were recruited between 1999 and 2001 and followed for 12 years. At baseline and every 2 years, dementia was suspected on the basis of the neuropsychological and neurological examination and confirmed by an independent committee of clinicians. Exposure to NO2, BC and PM2.5 at the participants’ residential address was estimated using land use regression models. For each pollutant and year of follow-up, the 10-year moving average of past exposure was estimated. Multilevel spatial random-effects Cox proportional hazards models were used in which exposure was included as a time-varying variable. Analyses were adjusted for individual (age, sex, education, APOE4 genotype, health behaviours) and contextual (neighbourhood deprivation index) confounders. ResultsAt baseline, the median age of the 7066 participants was 73.4 years, and 62% were women. The median follow-up duration was 10.0 years during which 791 participants developed dementia (n = 541 Alzheimer’s disease (AD) and n = 155 vascular/mixed dementia (VaD)). The 10-year moving average of PM2.5 concentrations ranged from 14.6 to 31.3 µg/m3.PM2.5 concentration was positively associated with dementia risk: HR = 1.20, 95% CI (1.08–1.32) for all-cause dementia, 1.20 (1.09–1.32) for AD, and 1.33 (1.05–1.68) for VaD per 5 µg/m3 PM2.5 increase. No association was detected between NO2 or BC exposure and dementia risk. ConclusionIn this large cohort of older adults, long-term PM2.5 exposure was associated with increased dementia incidence. Reducing PM2.5 emissions might lessen the burden of dementia in aging populations.

Design, Synthesis and Biological Evaluation of New Cycloalkyl Fused Quinolines Tethered to Isatin Schiff Bases as Cholinesterase Inhibitors.

Alzheimer's disease is now a most prevalent neurodegenerative disease of central nervous system leading to dementia in elderly population. Numerous pathological changes have been associated in the progression of Alzheimer's disease. One of such pathological hypotheses is declined cholinergic activity which eventually leads to cognitive and memory deficits. Inhibition o f cholinesterases will apparently elevate acetyl choline levels which is benefactor on cognitive symptoms of the disease. This manuscript describes the new tacrine derivatives tethered to isatin Schiff bases through alkanoyl linker and screened for cholinesterase inhibitory activity. Tacrine and two more cycloalkyl ring fused quinolones were synthesized and converted to N-cycloalkyl fused quinoline chloroamides. Isatin Schiff bases were also synthesized by the reaction between isatin and substituted aromatic anilines and in subsequent reaction, isatin Schiff bases were reacted with cycloalkyl fused quinolones to afford anticipated compounds 10a-i, 11a-i and 12a-i. All the compounds have been screened for acetyl- and butyrylcholinesterase inhibitory activity and in vivo behavioral studies. Binding interactions of the desired compounds have also been studied by docking them in active site of both cholinesterases. Three compounds 12d, 12e and 12h with propionyl and butyroyl linker between amine and isatin Schiff base scaffold have shown potent acetyl- and butyrylcholinesterase inhibitory activity. However most potent cholinesterase inhibitor was 13d with IC50 value of 0.71±0.004 and 1.08±0.02 μM against acetyl- and butyrylcholinesterases respectively. The hepatotoxicity of potent compounds revealed that the tested compounds were less hepatotoxic than tacrine and also exhibited encouraging in vivo behavioral studies in test animals. Docking studies of all the molecules disclosed close hydrogen bond interactions within the binding site of both cholinesterases. New cycloalkyl fused quinolones tethered with alkanoyl linker to isatin Schiff bases endowed significant and potent cholinesterase inhibitory activities. Few of the compounds have also exhibited lesser hepatotoxicity and all the synthesized compounds were good in behavioral studies. Molecular docking studies also indicated close interactions in active site of cholinesterases.

Liver Growth Factor "LGF" as a Therapeutic Agent for Alzheimer's Disease.

Alzheimer’s disease (AD) is a progressive degenerative disorder and the most common cause of dementia in aging populations. Although the pathological hallmarks of AD are well defined, currently no effective therapy exists. Liver growth factor (LGF) is a hepatic albumin–bilirubin complex with activity as a tissue regenerating factor in several neurodegenerative disorders such as Parkinson’s disease and Friedreich’s ataxia. Our aim here was to analyze the potential therapeutic effect of LGF on the APPswe mouse model of AD. Twenty-month-old mice received intraperitoneal (i.p.) injections of 1.6 µg LGF or saline, twice a week during three weeks. Mice were sacrificed one week later, and the hippocampus and dorsal cortex were prepared for immunohistochemical and biochemical studies. LGF treatment reduced amyloid-β (Aβ) content, phospho-Tau/Tau ratio and the number of Aβ plaques with diameter larger than 25 µm. LGF administration also modulated protein ubiquitination and HSP70 protein levels, reduced glial reactivity and inflammation, and the expression of the pro-apoptotic protein Bax. Because the administration of this factor also restored cognitive damage in APPswe mice, we propose LGF as a novel therapeutic tool that may be useful for the treatment of AD.

On the use of AI for Generation of Functional Music to Improve Mental Health.

Increasingly music has been shown to have both physical and mental health benefits including improvements in cardiovascular health, a link to reduction of cases of dementia in elderly populations, and improvements in markers of general mental well-being such as stress reduction. Here, we describe short case studies addressing general mental well-being (anxiety, stress-reduction) through AI-driven music generation. Engaging in active listening and music-making activities (especially for at risk age groups) can be particularly beneficial, and the practice of music therapy has been shown to be helpful in a range of use cases across a wide age range. However, access to music-making can be prohibitive in terms of access to expertize, materials, and cost. Furthermore the use of existing music for functional outcomes (such as targeted improvement in physical and mental health markers suggested above) can be hindered by issues of repetition and subsequent over-familiarity with existing material. In this paper, we describe machine learning approaches which create functional music informed by biophysiological measurement across two case studies, with target emotional states at opposing ends of a Cartesian affective space (a dimensional emotion space with points ranging from descriptors from relaxation, to fear). Galvanic skin response is used as a marker of psychological arousal and as an estimate of emotional state to be used as a control signal in the training of the machine learning algorithm. This algorithm creates a non-linear time series of musical features for sound synthesis “on-the-fly”, using a perceptually informed musical feature similarity model. We find an interaction between familiarity and perceived emotional response. We also report on subsequent psychometric evaluation of the generated material, and consider how these - and similar techniques - might be useful for a range of functional music generation tasks, for example, in nonlinear sound-tracking such as that found in interactive media or video games.

Abstract 13806: Catheter Ablation Improves Quasar-Arterial Spin Labeling Based Regional Brain Perfusion in the Posterior Cingulate Cortex and Auditory-verbal Memory Function in Elderly Patients With Atrial Fibrillation

Introduction: Recent epidemiological studies suggest that atrial fibrillation (AF) is a risk factor for cognitive decline and dementia in elderly population, which may be attributable to reduced stroke volume and related brain hypoperfusion as a potential cause. Catheter ablation therapy is an option for radical cure of AF. Although several researchers mentioned the possibility to improve cognition after the intervention, specific topographic features of the brain perfusion have not been well investigated. Hypothesis: To visualize hemodynamic alteration in regional cerebra blood flow (rCBF) associated with catheter ablation therapy using noninvasive MRI voxel-based analysis method and to clarify the relationship between AF and cognitive decline. Methods: Eight patients with persistent AF (2 male, average age 63.4±7.3) underwent noninvasive brain MRI perfusion imaging with a novel dynamic model-free arterial spin-labeling (ASL) technique (quantitative STAR labeling of arterial regions [QUASAR]) and cognitive tests including Mini-Mental State Exam (MMSE) and Ray Auditory Verbal Learning Test (RAVLT) before and after 6-months of intervention. QUASAR-ASL images were spatially normalized with SPM 12 applied by partial volume correction, followed by comparison of rCBF of each brain areas with voxel-based paired-t test. Results: After the ablation therapy, QUASAR-ASL showed significantly increased rCBF in the left posterior cingulate gyrus (PCC) (FWE, P &lt; 0.05, MNI coordinates = -9 -45 5, Figure), which was accompanied by improved scores of the RAVLT ( P &lt; 0.001). Conclusions: The PCC is a critical part of the limbic system initially affected focal energy metabolism by Alzheimer’s disease. Improved rCBF in left PCC in patients with AF after catheter ablation therapy, as demonstrated by QUASAR-ASL method, may prevent episodic memory decline related to the auditory-verbal cognitive function.

The Mexican Cognitive Aging Ancillary Study (Mex-Cog): Study Design and Methods

ObjectiveDescribe the protocol sample and instruments of the Cognitive Aging Ancillary Study in Mexico (Mex-Cog). The study performs an in-depth cognitive assessment in a subsample of older adults of the ongoing Mexican Health and Aging Study (MHAS). The Mex-Cog is part of the Harmonized Cognitive Assessment Protocol (HCAP) design to facilitate cross-national comparisons of the prevalence and trends of dementia in aging populations around the world, funded by the National Institute on Aging (NIA). MethodsThe study protocol consists of a cognitive assessment instrument for the target subject and an informant questionnaire. All cognitive measures were selected and adapted by a team of experts from different ongoing studies following criteria to warrant reliable and comparable cognitive instruments. The informant questionnaire is from the 10/66 Dementia Study in Mexico. ResultsA total of 2,265 subjects aged 55-104 years participated, representing a 70% response rate. Validity analyses showed the adequacy of the content validity, proper quality-control procedures that sustained data integrity, high reliability, and internal structure. ConclusionsThe Mex-Cog study provides in-depth cognitive data that enhances the study of cognitive aging in two ways. First, linking to MHAS longitudinal data on cognition, health, genetics, biomarkers, economic resources, health care, family arrangements, and psychosocial factors expands the scope of information on cognitive impairment and dementia among Mexican adults. Second, harmonization with other similar studies around the globe promotes cross-national studies on cognition with comparable data. Mex-Cog data is publicly available at no cost to researchers.

A study on prevalence of dementia among elderly population in rural health training centre field practice area of Nalgonda

Background: Dementia is one of the major causes of disability and dependency among older people worldwide. Dementia has physical, psychological, social and economic impact. Worldwide prevalence of dementia in elderly population of more than 60 years is 5-8%. Prevalence of mild cognitive impairment in India is 14.89%. Present study aim was to estimate the prevalence of dementia and the risk factors associated with dementia among elderly population in rural field practice area of Nalgonda district.Methods: A descriptive, community based cross-sectional study was conducted among 119 elderly population in the field practice area of Rural Health Training Centre by simple random sampling method, with the help of a pre-designed and pre-tested questionnaire. Data was analyzed using SPSS Version 19. MMSE (mini mental status examination) questionnaire was used to screen for dementia. Barthel index was used to assess the dependency status.Results: Demographic profile of the study population of 119, males 65 (54.62%), females 54 (45.38%). Majority of their source of income were government service pension 30 (25.21%) and old age pension 70 (58.82%). 56 (47.06%) of elderly population living with family and 63 (52.94%) people were living individually. The study revealed the prevalence of cognitive impairment is 35.3%. Risk factors like middle age obesity, smoking, alcohol consumption, social isolation showed significant association with dementia.Conclusions: Dementia can be prevented by early diagnosis and promoting physical health and treating behavioural and psychological symptoms. Risk of dementia can be reduced by following regular exercise, diet, quitting smoking and alcohol.

Prevalence of Risk Factors for Dementia in Elderly Population in a Tribal Area of Central India – A Community-Based Cross-Sectional Study

Prevalence of Risk Factors for Dementia in Elderly Population in a Tribal Area of Central India – A Community-Based Cross-Sectional Study

Circulating Vitamin D Levels and Alzheimer's Disease: A Mendelian Randomization Study in the IGAP and UK Biobank.

Observational studies strongly supported the association of low levels of circulating 25-hydroxyvitamin D (25OHD) and cognitive impairment or dementia in aging populations. However, randomized controlled trials have not shown clear evidence that vitamin D supplementation could improve cognitive outcomes. In fact, some studies reported the association between vitamin D and cognitive impairment based on individuals aged 60 years and over. However, it is still unclear that whether vitamin D levels are causally associated with Alzheimer's disease (AD) risk in individuals aged 60 years and over. Here, we performed a Mendelian randomization (MR) study to investigate the causal association between vitamin D levels and AD using a large-scale vitamin D genome-wide association study (GWAS) dataset and two large-scale AD GWAS datasets from the IGAP and UK Biobank with individuals aged 60 years and over. Our results showed that genetically increased 25OHD levels were significantly associated with reduced AD risk in individuals aged 60 years and over. Hence, our findings in combination with previous literature indicate that maintaining adequate vitamin D status in older people especially aged 60 years and over, may contribute to slow down cognitive decline and forestall AD. Long-term randomized controlled trials are required to test whether vitamin D supplementation may prevent AD in older people especially those aged 60 years and may be recommended as preventive agents.

Prevention of dementia in elderly population: A comprehensive review of literature

Background and Aims: Dementia is the loss of cognitive functioning – remembering, thinking, and reasoning – and behavioral capabilities to such a degree that it interferes with an individual's daily living activities. The objective of this paper is to summarize current knowledge on the most promising interventions for preventing cognitive decline. Methods: Electronic databases were searched using PubMed/Medline and Google Scholar to retrieve relevant research papers conducted in Saudi Arabia and internationally. Keywords included “dementia,” “prevention strategies,” “aging,” “aged,” “Elderly population.” Articles published in the English language and published between 2000 and 2018 were included in the study. Analysis: Overall, limited evidence exists to support the cause-effect association between the progression/development of dementia and preventative strategies. Studies to date provide the most promising strategies for dementia prevention that includes healthy diet, social engagement, physical activity, cognitive activity, and vascular risk factor control. Conclusion: Dementia is a disease more commonly observed in old people. Studies in the future will determine the risk factor modification and its implications in controlled trials with specific emphasis on whether some simultaneous interventions may either have a multiplicative or additive effect.