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Hypovitaminosis D, a common condition in older adults, is associated with brain changes and dementia. Given the fast growing contribution of literature in this research field, clear guidance is needed for clinicians and researchers. International experts met at the invitational summit on "Vitamin D and cognition in older adults" in Boston, MA, July 2013. Based upon literature and expert opinion, the task force focused on key questions on the role of vitamin D in Alzheimer disease and related disorders. Each question was discussed and voted using a Delphi-like approach. Experts reached agreement that hypovitaminosis D increases the risk of cognitive decline and dementia in older adults, may alter the clinical presentation as a consequence of related comorbidities, but should not be used thus far as a diagnostic or prognostic biomarker of Alzheimer disease due to lack of specificity and insufficient evidence. Hypovitaminosis D should be screened in this population because of its high prevalence and supplemented, if necessary, but this advice was not specific to cognition. The task force agreed on 5 overarching principles related to vitamin D and cognition in older adults.

Background: Parental longevity confers lower risks for some age-related diseases in offspring. We tested the association between parental longevity and late-life cognitive decline or dementia., Methods: Data were from the Health and Retirement Study (HRS), a US national sample. Biennial cognitive assessment (Telephone Interview of Cognitive Status-Modified [TICS-m]) occurred for ages 64 years or older in 1996 through 2008 (maximum, 79 years), including physician-diagnosed memory disorder. Offspring were categorized into parental longevity groups based on gender-specific distributional cut points. Model covariates included race, respondents' education, and income status during childhood and adulthood., Results: Offspring groups did not differ on TICS-m scores at baseline. During follow-up, offspring of two long-lived parents experienced 40% slower rates of TICS-m decline than those with no long-lived parents (95% confidence interval, 12-72; P=.003; n=4731). Increased parental longevity was also associated with lower risk of physician-diagnosed memory disorder. Estimates did not change after controlling for environmental variables., Conclusions: Parental longevity is associated inversely with cognitive decline and self-reported diagnosed memory disorders in aging offspring. Parental longevity may be a valuable trait for identifying early biomarkers for resistance to cognitive decline in aging., (Copyright © 2014 The Alzheimer's Association. Published by Elsevier Inc. All rights reserved.)

Objective: To assess the effects of a history of alcohol use disorders (AUDs) on risk of severe cognitive and memory impairment in later life., Methods: We studied the association between history of AUDs and the onset of severe cognitive and memory impairment in 6,542 middle-aged adults born 1931 through 1941 who participated in the Health and Retirement Study, a prospective nationally representative U.S. cohort. Participants were assessed at 1992 baseline and follow-up cognitive assessments were conducted biannually from 1996 through 2010. History of AUDs was identified using the three-item modified CAGE questionnaire. Cognitive outcomes were assessed using the 35-item modified Telephone Interview for Cognitive Status at last follow-up with incident severe cognitive impairment defined as a score ≤ 8, and incident severe memory impairment defined as a score ≤ 1 on a 20-item memory subscale., Results: During up to 19 years of follow-up (mean: 16.7 years, standard deviation: 3.0, range: 3.5-19.1 years), 90 participants experienced severe cognitive impairment and 74 participants experienced severe memory impairment. History of AUDs more than doubled the odds of severe memory impairment (odds ratio [OR] = 2.21, 95% confidence interval [CI] = 1.27-3.85, t = 2.88, df = 52, p = 0.01). The association with severe cognitive impairment was statistically non-significant but in the same direction (OR = 1.80, 95% CI = 0.97-3.33, t = 1.92, df = 52, p = 0.06)., Conclusion: Middle-aged adults with a history of AUDs have increased odds of developing severe memory impairment later in life. These results reinforce the need to consider the relationship between alcohol consumption and cognition from a multifactorial lifespan perspective., (Copyright © 2014 American Association for Geriatric Psychiatry. Published by Elsevier Inc. All rights reserved.)

Objective: To examine the association between cognitive function and dementia with vitamin D concentration in adults., Methods: Five databases were searched for English-language studies up to August 2010, and included all study designs with a comparative group. Cognitive function or impairment was defined by tests of global or domain-specific cognitive performance and dementia was diagnosed according to recognized criteria. A vitamin D measurement was required. Two authors independently extracted data and assessed study quality using predefined criteria. The Q statistic and I² methods were used to test for heterogeneity. We conducted meta-analyses using random effects models for the weighted mean difference (WMD) and Hedge's g., Results: Thirty-seven studies were included; 8 contained data allowing mean Mini-Mental State Examination (MMSE) scores to be compared between participants with vitamin D <50 nmol/L to those with values ≥50 nmol/L. There was significant heterogeneity among the studies that compared the WMD for MMSE but an overall positive effect for the higher vitamin D group (1.2, 95% confidence interval [CI] 0.5 to 1.9; I² = 0.65; p = 0.002). The small positive effect persisted despite several sensitivity analyses. Six studies presented data comparing Alzheimer disease (AD) to controls but 2 utilized a method withdrawn from commercial use. For the remaining 4 studies the AD group had a lower vitamin D concentration compared to the control group (WMD = -6.2 nmol/L, 95% CI -10.6 to -1.8) with no heterogeneity (I² < 0.01; p = 0.53)., Conclusion: These results suggest that lower vitamin D concentrations are associated with poorer cognitive function and a higher risk of AD. Further studies are required to determine the significance and potential public health benefit of this association.

Introduction: Circulating inflammatory markers may play an important role in cognitive impairment at older ages. Mice deficient for the chemokine (C-C motif) receptor 2 (CCR2) develop an accelerated Alzheimer-like pathology. CCR2 is also important in neurogenesis. To identify human gene transcripts most closely associated with Mini-Mental State Examination (MMSE) scores, we undertook a genome-wide and inflammation specific transcriptome screen in circulating leukocytes from a population-based sample., Methods: We measured in vivo transcript levels by microarray analysis in 691 subjects (mean age 72.6 years) in the InCHIANTI study (Invecchiare in Chianti, aging in the Chianti area). We assessed expression associations with MMSE performance at RNA collection and prior 9-year change in MMSE score in linear regression models., Results: In genome-wide analysis, raised CCR2 expression was cross-sectionally the most strongly associated transcript with lower MMSE score (beta=-0.16, p=5.1×10(-6), false discovery rate (FDR; q=0.077). Amongst inflammatory transcripts, only CCR2 expression was associated with both MMSE score and accelerated decline in score over the preceding 9 years (beta=-0.16, p=5.1×10(-6), q=0.003; and beta=-0.13, p=5.5×10(-5), q=0.03, respectively). CCR2 expression was also positively associated with apolipoprotein E (ApoE) e4 Alzheimer disease risk haplotype., Conclusions: We show for the first time that CCR2 expression is associated with lower MMSE scores in an older human population. Laboratory models of Ccr2-mediated β-amyloid removal and regulation of neurogenesis affecting cognitive function may be applicable in humans. CCR2-mediated pathways may provide a possible focus for intervention to potentiate protective reactions to Alzheimer pathology in older people, including for people with an adverse ApoE haplotype.

The physiologically active form of vitamin D, 1,25-dihydroxyvitamin D(3), is a fat-soluble steroid hormone with a well established role in skeletal health. A growing body of evidence suggests low vitamin D levels also play a role in the pathogenesis of a wide range of non-skeletal, age-associated diseases including cancer, heart disease, type 2 diabetes mellitus and stroke. Low levels of serum 25-hydroxyvitamin D [25(OH)D], a stable marker of vitamin D status, are also associated with increased odds of prevalent cognitive dysfunction, Alzheimer's disease and all-cause dementia in a number of studies, raising the possibility that vitamin D plays a role in the aetiology of cognitive dysfunction and dementia. To date, the majority of human studies reporting associations between vitamin D and cognition or dementia have been cross-sectional or case-control designs that do not permit us to exclude the possibility that such associations are a result of disease progression rather than being causal. Animal and in vitro experiments have identified a number of neuroprotective mechanisms that might link vitamin D status to cognitive dysfunction and dementia, including vasoprotection and amyloid phagocytosis and clearance, but the clinical relevance of these mechanisms in humans is not currently clear. Two recent, large, prospective studies go some way to establish the temporal relationship with cognitive decline. The relative risk of cognitive decline was 60% higher (relative risk = 1.6, 95% CI 1.2, 2.0) in elderly Italian adults with severely deficient 25(OH)D levels (<25 nmol/L) when compared with those with sufficient levels (≥75 nmol/L). Similarly, the odds of cognitive decline were 41% higher (odds ratio = 1.4, 95% CI 0.9, 2.2) when elderly US men in the lowest quartile (≤49.7 nmol/L) were compared with those in the highest quartile (≥74.4 nmol/L). To our knowledge, no prospective studies have examined the association between 25(OH)D levels and incident dementia or neuroimaging abnormalities. The possible therapeutic benefits of vitamin D have attracted considerable interest as over 1 billion people worldwide are thought to have insufficient 25(OH)D levels and these levels can be increased using inexpensive and well tolerated dietary supplements. However, no large randomized controlled trials have yet examined the effect of vitamin D supplements on cognitive decline or incident dementia. Further studies are urgently needed to establish which mechanisms have clinical relevance in human populations and whether vitamin D supplements are effective at minimizing cognitive decline or preventing dementia.

Objectives: To compare the characteristics and outcomes of caregivers of adults with dementia with those of caregivers of adults with cognitive impairment, not dementia (CIND)., Design: Cross-sectional., Setting: In-home assessment for cognitive impairment and self-administered caregiving questionnaire., Participants: One hundred sixty-nine primary family caregivers of participants in the Aging, Demographics, and Memory Study (ADAMS). ADAMS participants were aged 71 and older drawn from the nationally representative Health and Retirement Study., Measurements: Neuropsychological testing, neurological examination, clinical assessment, and medical history were used to assign a diagnosis of normal cognition, CIND, or dementia. Caregiving measures included caregiving time, functional limitations, depressive symptoms, physical and emotional strain, caregiving rewards, caregiver health, and demographic characteristics., Results: Dementia caregivers spent approximately 9 hours per day providing care, compared with 4 hours per day for CIND caregivers (P=.001). Forty-four percent of dementia caregivers exhibited depressive symptoms, compared with 26.5% of CIND caregivers (P=.03). Physical and emotional strains were similar in both groups of caregivers. Regardless of the strains, nearly all caregivers reported some benefits from providing care. Behavioral problems (P=.01) and difficulty with instrumental activities of daily living (P=.01) in persons with CIND partially explained emotional strain experienced by CIND caregivers. For those with dementia, behavioral problems predicted caregiver emotional strain (P<.001) and depressive symptoms (P=.01)., Conclusion: Although support services are available to dementia caregivers, CIND caregivers also expend considerable time and experience strains. The real caregiver burden of cognitive impairment in the U.S. population may therefore be greatly underestimated if people who have reached the diagnostic threshold for dementia are focused on exclusively., (© 2011, Copyright the Authors. Journal compilation © 2011, The American Geriatrics Society.)

Objectives: To examine the association between neuropsychiatric symptoms and risk of institutionalization and death., Design: Analysis of longitudinal data., Setting: The Aging, Demographics, and Memory Study (ADAMS)., Participants: Five hundred thirty-seven adults aged 71 and older with cognitive impairment drawn from the Health and Retirement Study (HRS)., Measurements: Neuropsychiatric symptoms (delusions, hallucinations, agitation, depression, apathy, elation, anxiety, disinhibition, irritation, and aberrant motor behaviors) and caregiver distress were identified using the Neuropsychiatric Inventory. A consensus panel in the ADAMS assigned cognitive category. Date of nursing home placement and information on death, functional limitations, medical comorbidity, and sociodemographic characteristics were obtained from the HRS and ADAMS., Results: Overall, the presence of one or more neuropsychiatric symptoms was not associated with a significantly higher risk for institutionalization or death during the 5-year study period, although when assessing each symptom individually, depression, delusions, and agitation were each associated with a significantly higher risk of institutionalization (hazard rate (HR)=3.06, 95% confidence interval (CI)=1.09-8.59 for depression; HR=5.74, 95% CI=1.94-16.96 for clinically significant delusions; HR=4.70, 95% CI=1.07-20.70 for clinically significant agitation). Caregiver distress mediated the association between delusions and agitation and institutionalization. Depression and hallucinations were associated with significantly higher mortality (HR=1.56, 95% CI=1.08-2.26 for depression; HR=2.59, 95% CI=1.09-6.16 for clinically significant hallucinations)., Conclusion: Some, but not all, neuropsychiatric symptoms are associated with a higher risk of institutionalization and death in people with cognitive impairment, and caregiver distress also influences institutionalization. Interventions that better target and treat depression, delusions, agitation, and hallucinations, as well as caregiver distress, may help delay or prevent these negative clinical outcomes., (© 2011, Copyright the Authors. Journal compilation © 2011, The American Geriatrics Society.)

Background: Recent European studies suggest that vitamin D deficiency may be associated with increased odds of cognitive impairment in older persons, although findings from the United States are equivocal. Our objective was to investigate the association between vitamin D deficiency and cognitive impairment in the elderly U.S. population., Methods: Three thousand and three hundred twenty-five adults aged 65 years or more completed cognitive assessments, medical examinations, and physical performance measures and provided blood samples in the Third National Health and Nutrition Examination Survey, a nationally representative cross-sectional study of the U.S. noninstitutionalized population. We determined whether low levels of serum 25-hydroxyvitamin D (25(OH)D) were associated with increased odds of cognitive impairment using logistic regression models. Cognitive impairment was assessed using measures of immediate and delayed verbal memory, orientation, and attention (impairment was defined as the worst 10% of the distribution of combined scores)., Results: The multivariate adjusted odds ratios (95% confidence interval) of cognitive impairment in participants who were 25(OH)D insufficient (≥ 50 < 75 nmol/L), deficient (≥ 25 < 50 nmol/L), and severely deficient (<25 nmol/L) in comparison with those sufficient (≥ 75 nmol/L) were 0.9 (0.6-1.3), 1.4 (1.0-2.1), and 3.9 (1.5-10.4), respectively (p for linear trend = .02). Log-transformed levels of 25(OH)D were also significantly associated with the odds of cognitive impairment (p = .02)., Conclusions: These findings suggest that vitamin D deficiency is associated with increased odds of cognitive impairment in the elderly U.S. population. Further exploration of a possible causal relationship between vitamin D deficiency and cognitive impairment is warranted.

A recent genome-wide association (GWA) study of late-onset Alzheimer's disease (LOAD) identified 15 novel single nucleotide polymorphisms (SNPs) independent of ApoE. We hypothesised that variants associated with LOAD are also associated with poor cognitive function in elderly populations. We measured additive associations between the five most strongly associated LOAD SNPs and grouped Mini Mental State Examination (MMSE) scores. Variants were genotyped in respondents (mean age 79 years) from the Oxford Healthy Ageing project (OHAP) and other sites of the MRC Cognitive Function and Ageing Study (MRC-CFAS). In adjusted ordinal logistic models, two variants were associated with poorer cognitive function: rs11622883 (OR=1.14, 95% CI: 1.01-1.28, p=0.040) and rs505058 (OR=1.29, 95% CI: 1.02-1.64, p=0.036). These SNPs are close to a SERPINA gene cluster and within LMNA, respectively. The mechanisms underlying the associations with cognitive impairment and LOAD require further elucidation, but both genes are interesting candidates for involvement in age-related cognitive impairment., (Copyright 2008 Elsevier Inc. All rights reserved.)

Background: To our knowledge, no prospective study has examined the association between vitamin D and cognitive decline or dementia., Methods: We determined whether low levels of serum 25-hydroxyvitamin D (25[OH]D) were associated with an increased risk of substantial cognitive decline in the InCHIANTI population-based study conducted in Italy between 1998 and 2006 with follow-up assessments every 3 years. A total of 858 adults 65 years or older completed interviews, cognitive assessments, and medical examinations and provided blood samples. Cognitive decline was assessed using the Mini-Mental State Examination (MMSE), and substantial decline was defined as 3 or more points. The Trail-Making Tests A and B were also used, and substantial decline was defined as the worst 10% of the distribution of decline or as discontinued testing., Results: The multivariate adjusted relative risk (95% confidence interval [CI]) of substantial cognitive decline on the MMSE in participants who were severely serum 25(OH)D deficient (levels <25 nmol/L) in comparison with those with sufficient levels of 25(OH)D (>/=75 nmol/L) was 1.60 (95% CI, 1.19-2.00). Multivariate adjusted random-effects models demonstrated that the scores of participants who were severely 25(OH)D deficient declined by an additional 0.3 MMSE points per year more than those with sufficient levels of 25(OH)D. The relative risk for substantial decline on Trail-Making Test B was 1.31 (95% CI, 1.03-1.51) among those who were severely 25(OH)D deficient compared with those with sufficient levels of 25(OH)D. No significant association was observed for Trail-Making Test A., Conclusion: Low levels of vitamin D were associated with substantial cognitive decline in the elderly population studied over a 6-year period, which raises important new possibilities for treatment and prevention.

Objectives: To estimate the prevalence of neuropsychiatric symptoms and examine their association with functional limitations., Design: Cross-sectional analysis., Setting: The Aging, Demographics, and Memory Study (ADAMS)., Participants: A sample of adults aged 71 and older (N=856) drawn from Health and Retirement Study (HRS), a nationally representative cohort of U.S. adults aged 51 and older., Measurements: The presence of neuropsychiatric symptoms (delusions, hallucinations, agitation, depression, apathy, elation, anxiety, disinhibition, irritation, and aberrant motor behaviors) was identified using the Neuropsychiatric Inventory. A consensus panel in the ADAMS assigned a cognitive category (normal cognition; cognitive impairment, no dementia (CIND); mild, moderate, or severe dementia). Functional limitations, chronic medical conditions, and sociodemographic information were obtained from the HRS and ADAMS., Results: Forty-three percent of individuals with CIND and 58% of those with dementia exhibited at least one neuropsychiatric symptom. Depression was the most common individual symptom in those with normal cognition (12%), CIND (30%), and mild dementia (25%), whereas apathy (42%) and agitation (41%) were most common in those with severe dementia. Individuals with three or more symptoms and one or more clinically significant symptoms had significantly higher odds of having functional limitations. Those with clinically significant depression had higher odds of activity of daily living limitations, and those with clinically significant depression, anxiety, or aberrant motor behaviors had significantly higher odds of instrumental activity of daily living limitations., Conclusion: Neuropsychiatric symptoms are highly prevalent in older adults with CIND and dementia. Of those with cognitive impairment, a greater number of total neuropsychiatric symptoms and some specific individual symptoms are strongly associated with functional limitations.

Objective: This study presents an in-depth neuropsychological study of the consequences of a survivable transoral penetrating gunshot injury resulting in lesions to frontal lobe structures., Design: A case study of a woman who sustained a self-inflicted transoral gunshot injury that resulted in focal pathology to the frontal lobes., Methods: Neuropsychological examination with a comprehensive battery of standard tests., Results: Striking contrasts in performance were found on tests of executive function relating to planning and problem-solving ability, with marked impairment on a problem-solving task involving an action plan. Intact performance was seen on tests of memory., Conclusions: This case study demonstrates that transoral gunshot injury to the brain is survivable, though selective executive dysfunction may remain.

Background: The diagnosis of cognitive impairment and dementia must reflect an increasingly diverse and aging United States population. This study compared direct testing and informant reports of cognition with clinical diagnoses of cognitive impairment and dementia between African Americans and whites., Methods: Participants in the Aging, Demographics, and Memory Study completed in-person dementia evaluations, and were assigned clinical diagnoses (by a consensus panel of dementia experts) of normal; cognitive impairment, not demented (CIND); and dementia. The Consortium to Establish a Registry for Alzheimer's Disease (CERAD) total score and the Informant Questionnaire on Cognitive Decline in the Elderly (IQCODE) were used to assess cognitive performance and reported cognitive decline., Results: A higher CERAD total score was associated with lower odds of CIND and dementia, at comparable ratios between African Americans and whites. Higher IQCODE scores were associated with increased odds of dementia in both African Americans and whites. Higher IQCODE scores were associated with increased odds of CIND among whites, but not among African Americans., Conclusions: Cultural differences may influence informant reports of prevalent CIND and dementia. Our findings also highlight the need for more comparative research to establish the cultural validity of measures used to diagnose these conditions.

Vitamin D may be of interest in the prevention of cognitive impairment, though previous findings are inconclusive. Participants were 1766 adults aged 65 years and older from the Health Survey for England 2000, a nationally representative population-based study. Cognitive impairment was assessed using the Abbreviated Mental Test Score. The cross-sectional relation of serum 25-hydroxyvitamin D quartiles to cognitive impairment was modeled using logistic regression. In all, 212 participants (12%) were cognitively impaired. Odds ratios (95% confidence intervals) for cognitive impairment in the first (8-30 nmol/L), second (31-44 nmol/L), and third (45-65 nmol/L) quartiles of serum 25-hydroxyvitamin D compared with the fourth (66-170 nmol/L) were 2.3 (1.4-3.8), 1.4 (0.8-2.4), and 1.1 (0.6-1.9), after adjustment for age, sex, education, ethnicity, season of testing, and additional risk factors for cognitive impairment (P for linear trend = .001). Our data suggest low serum 25-hydroxyvitamin D is associated with increased odds of cognitive impairment.

Background: Cognitive function is a key determinant of independence and quality of life among older adults. Compared to adults in England, US adults have a greater prevalence of cardiovascular risk factors and disease that may lead to poorer cognitive function. We compared cognitive performance of older adults in the US and England, and sought to identify sociodemographic and medical factors associated with differences in cognitive function between the two countries., Methods: Data were from the 2002 waves of the US Health and Retirement Study (HRS) (n = 8,299) and the English Longitudinal Study of Ageing (ELSA) (n = 5,276), nationally representative population-based studies designed to facilitate direct comparisons of health, wealth, and well-being. There were differences in the administration of the HRS and ELSA surveys, including use of both telephone and in-person administration of the HRS compared to only in-person administration of the ELSA, and a significantly higher response rate for the HRS (87% for the HRS vs. 67% for the ELSA). In each country, we assessed cognitive performance in non-hispanic whites aged 65 and over using the same tests of memory and orientation (0 to 24 point scale)., Results: US adults scored significantly better than English adults on the 24-point cognitive scale (unadjusted mean: 12.8 vs. 11.4, P < .001; age- and sex-adjusted: 13.2 vs. 11.7, P < .001). The US cognitive advantage was apparent even though US adults had a significantly higher prevalence of cardiovascular risk factors and disease. In a series of OLS regression analyses that controlled for a range of sociodemographic and medical factors, higher levels of education and wealth, and lower levels of depressive symptoms, accounted for some of the US cognitive advantage. US adults were also more likely to be taking medications for hypertension, and hypertension treatment was associated with significantly better cognitive function in the US, but not in England (P = .014 for treatment x country interaction)., Conclusion: Despite methodological differences in the administration of the surveys in the two countries, US adults aged >/= 65 appeared to be cognitively healthier than English adults, even though they had a higher burden of cardiovascular risk factors and disease. Given the growing number of older adults worldwide, future cross-national studies aimed at identifying the medical and social factors that might prevent or delay cognitive decline in older adults would make important and valuable contributions to public health.

Objective: To examine the association between a biomarker of exposure to secondhand smoke (salivary cotinine concentration) and cognitive impairment., Design: Cross sectional analysis of a national population based study., Setting: Stratified random sample of households throughout England., Participants: 4809 non-smoking adults aged 50 years or more from the 1998, 1999, and 2001 waves of the Health Survey for England who also participated in the 2002 wave of the English Longitudinal Study of Ageing and provided saliva samples for cotinine assay and a detailed smoking history., Main Outcome Measure: Cognitive impairment as defined by the lowest 10% of scores on a battery of neuropsychological tests., Results: Participants who did not smoke, use nicotine products, or have salivary cotinine concentrations of 14.1 ng/ml or more were divided into four equal size groups on the basis of cotinine concentrations. Compared with the lowest fourth of cotinine concentration (0.0-0.1 ng/ml) the odds ratios (95% confidence intervals) for cognitive impairment in the second (0.2-0.3 ng/ml), third (0.4-0.7 ng/ml), and highest fourths (0.8-13.5 ng/ml) were 1.08 (0.78 to 1.48), 1.13 (0.81 to 1.56), and 1.44 (1.07 to 1.94; P for trend 0.02), after adjustment for a wide range of established risk factors for cognitive impairment. A similar pattern of associations was observed for never smokers and former smokers., Conclusions: Exposure to secondhand smoke may be associated with increased odds of cognitive impairment. Prospective nationally representative studies relating biomarkers of exposure to cognitive decline and risk of dementia are needed.

Background: The relationship between stroke risk and cognitive function has not previously been examined in a large community living sample other than the Framingham cohort. The objective of this study was to examine the relationship between 10-year risk for incident stroke and cognitive function in a large population-based sample., Methods: Participants were 7377 adults aged 50 years and over of the 2002 wave of the English Longitudinal Study of Ageing, a prospective cohort study. A modified version of the Framingham Stroke Risk Profile (incorporating age, sex, systolic blood pressure, antihypertensive medication, diabetes, smoking status, cardiovascular disease, and atrial fibrillation) was used to assess 10-year risk of stroke. Linear regression models were used to determine the cross-sectional relationship of stroke risk to global cognitive function and performance in multiple cognitive domains., Results: In unadjusted models 10 percentage point increments of 10-year stroke risk were associated with poor global cognitive function (-0.40 SD units, 95% CI -0.43 - -0.38), and lowered performance in all cognitive domains. After statistical adjustment for age, sex, testing interval and other correlates of cognitive function the association with stroke risk was attenuated though remained significant for global cognitive function (-0.06 SD units, 95% CI -0.09 - -0.03), immediate and delayed verbal memory, semantic verbal fluency and processing speed., Conclusion: In individuals free from a history of stroke or dementia, high subclinical cerebrovascular disease burden was associated with worse cognitive function in multiple domains.

Objectives: To assess the relationship between cognitive function, socioeconomic status, and neighborhood deprivation (lack of local resources of all types, financial and otherwise)., Design: Nationally representative cross-section., Setting: The English Longitudinal Study of Ageing (ELSA)., Participants: Seven thousand one hundred twenty-six community-dwelling individuals aged 52 and older and resident in urban areas., Measurements: Individual cognitive function score and index of multiple deprivation (IMD) at the Super Output Area level, adjusting for health, lifestyle, and sociodemographic confounders. Analyses were conducted separately according to sex and age group (52-69 and > or = 70)., Results: IMD affected cognitive function independent of the effects of education and socioeconomic status. For example, in fully adjusted models, women aged 70 and older had a standardized cognitive function score (z-score) that was 0.20 points (95% confidence interval (CI)=0.01-0.39) lower in the bottom 20% of wealth than the top 20%, 0.44 points (95% CI=0.20-0.69) lower in the least-educated group than in the most educated, and 0.31 points (95% CI 0.15-0.48) lower if resident lived in an area in the bottom 20% of IMD than in the top 20%., Conclusion: In community-based older people in urban neighborhoods, neighborhood deprivation--living in a neighborhood with high levels of deprivation, compared with national levels--is associated with cognitive function independent of individual socioeconomic circumstances. The mechanisms underlying this relationship are unclear and warrant further investigation.

Background: US studies suggest that leptin, a fat-derived hormone, may be protective against the development of dementia. Objective: To investigate the complex relationship between leptin levels and cognitive decline in elderly Italians. Methods: We studied circulating fasting leptin levels in 809 elderly adults free from dementia who participated in the prospective Italian population-based InCHIANTI study between 1998 and 2009 (mean follow-up of 8.0 years). Global cognitive decline was defined as a reduction of &nvge;5 points on the Mini-Mental State Examination (MMSE). Trail-Making Tests A and B were also incorporated, with cognitive decline defined as discontinued testing or the worst 10% of change from baseline. We also investigated whether any association could be explained by midlife weight and whether cognitive decline was associated with changing leptin levels. Results: The multivariate adjusted relative risk ([RR]; 95% confidence interval [CI]) of cognitive decline on the MMSE was 0.84 (95% CI 0.73-0.97) in relation to baseline sex-standardized log-leptin levels. High leptin levels showed a non-significant trend toward a reduced risk of decline on the Trail-Making Tests A (RR = 0.85, 95% CI 0.71-1.02) and B (RR = 0.90, 0.79-1.02). Adjusting for midlife weight or change in weight did not alter the pattern of results, and cognitive decline was not associated with changing leptin levels. Conclusions: High leptin levels were independently associated with a reduced risk of cognitive decline in elderly Italians. [ABSTRACT FROM AUTHOR]

Objective To examine the association between a biomarker of exposure to secondhand smoke (salivary cotinine concentration) and cognitive impairment. Design Cross sectional analysis of a national population based study. Setting Stratified random sample of households throughout England. Participants 4809 non-smoking adults aged 50 years or more from the 1998,1999, and 2001 waves of the Health Survey for England who also participated in the 2002 wave of the English Longitudinal Study of Ageing and provided saliva samples for cotinine assay and a detailed smoking history. Main outcome measure Cognitive impairment as defined by the lowest 10% of scores on a battery of neuropsychological tests. Results Participants who did not smoke, use nicotine products, or have salivary cotinine concentrations of 14.1 ng/ml or more were divided into four equal size groups on the basis of cotinine concentrations. Compared with the lowest fourth of cotinine concentration (0.0-0.1 ng/ml) the odds ratios (95% confidence intervals) for cognitive impairment in the second (0.2-0.3 ng/ml), third (0.4-0.7 ng/ml), and highest fourths (0.8-13.5 ng/ml) were 1.08 (0.78 to 1.48), 1.13 (0.81 to 1.56), and 1.44 (1.07 to 1.94; P for trend 0.02), after adjustment for a wide range of established risk factors for cognitive impairment. A similar pattern of associations was observed for never smokers and former smokers. Conclusions Exposure to secondhand smoke may be associated with increased odds of cognitive impairment. Prospective nationally representative studies relating biomarkers of exposure to cognitive decline and risk of dementia are needed. [ABSTRACT FROM AUTHOR]

The traditional Mediterranean diet (MedDiet), rich in minimally processed plant foods and fish, has been widely recognized to be one of the healthiest diets. Data from multiple randomized clinical trials have demonstrated its powerful effect against oxidative stress, inflammation and the development and progression of cardiovascular disease, type 2 diabetes, and other metabolic conditions that play a crucial role in the pathogenesis of neurodegenerative diseases. The protecting effects of the MedDiet against cognitive decline have been investigated in several observational and experimental studies. Data from observational studies suggest that the MedDiet may represent an effective dietary strategy for the early prevention of dementia, although these findings require further substantiation in clinical trials which have so far produced inconclusive results. Moreover, as we discuss in this review, accumulating data emphasizes the importance of: 1) maintaining an optimal nutritional and metabolic status for the promotion of healthy cognitive aging, and 2) implementing cognition-sparing dietary and lifestyle interventions during early time-sensitive windows before the pathological cascades turn into an irreversible state. In summary, components of the MedDiet pattern, such as essential fatty acids, polyphenols and vitamins, have been associated with reduced oxidative stress and the current evidence from observational studies seems to assign to the MedDiet a beneficial role in promoting brain health; however, results from clinical trials have been inconsistent. While we advocate for longitudinal analyses and for larger and longer clinical trials to be conducted, we assert our interim support to the use of the MedDiet as a protective dietary intervention for cognitive function based on its proven cardiovascular and metabolic benefits. [Display omitted] • Mediterranean diet is one of the most known health-promoting dietary patterns. • Mediterranean diet promotes the consumption of unrefined, plant-based foods. • Mediterranean diet increases the consumption of several nutrients with established anti-oxidant effects. • Mediterranean Diet has been associated with reduced cognitive decline. [ABSTRACT FROM AUTHOR]