Type 2 diabetes, depressive symptoms and trajectories of cognitive decline in a national sample of community-dwellers: a prospective cohort study

We examined the individual and synergistic effects of type 2 diabetes and elevated depressive symptoms on memory and executive function trajectories over 10 and eight years of follow-up, respectively. Our sample comprised 10,524 community-dwellers aged ≥50 years in 2002±03 from the English Longitudinal Study of Ageing. With respect to memory (word recall), participants with either diabetes or elevated depressive symptoms recalled significantly fewer words compared with those free of these conditions (reference category), but more words compared with those with both conditions. There was a significant acceleration in the rate of memory decline in participants aged ≤50±64 years with both conditions (-0.27, 95% CI, -0.45 to -0.08, per study wave), which was not observed in those with either condition or aged ≥65 years. With respect to executive function (animal naming), participants aged 65 years with diabetes or those with elevated depressive symptoms named significantly fewer animals compared with the reference category, while those with both conditions named fewer animals compared with any other category. The rate of executive function decline was significantly greater in participants with both conditions (-0.54, 95% CI, -0.99 to -0.10; and ±0.71, 95% CI, -1.16 to -0.27, per study wave, for those aged 50±64 and ≥65 years, respectively), but not in participants with either condition. Diabetes and elevated depressive symptoms are inversely associated with memory and executive function, but, individually, do not accelerate cognitive decline. The co-occurrence of diabetes and elevated depressive symptoms significantly accelerates cognitive decline over time, especially among those aged 50±64 years

Education, occupational class, and cognitive decline in preclinical dementia

We investigated education and occupational influences as markers of cognitive reserve in relation to cognitive performance and decline on multiple fluid and crystallized abilities in preclinical dementia. From the total sample of 702 participants stemming from the OCTO-Twin Study (Sweden), aged 80+ at baseline in 1992-1993, only those who developed dementia during the study period (N = 127) were included in these analyses. Random effects models were used to examine the level of performance at the time of dementia diagnosis and the rates of decline prior to diagnosis. The results demonstrated that both fluid and crystallized abilities decline in preclinical stages, and that education and occupational class have independent moderating roles on the cognitive performance at the time of diagnosis, but not on the rates of decline

An international evaluation of cognitive reserve and memory changes in early old age in ten European countries

BACKGROUND: Cognitive reserve was postulated to explain individual differences in susceptibility to ageing, offering apparent protection to those with higher education. We investigated the association between education and change in memory in early old age. METHODS: Immediate and delayed memory scores from over 10,000 individuals aged 65 years and older, from 10 countries of the Survey of Health, Ageing and Retirement in Europe (SHARE), were modeled as a function of time in the study over an 8-year period, fitting independent latent growth models (LGM). Education was used as a marker of cognitive reserve and evaluated in associations with memory performance and rate of change, while accounting for income, general health, smoking, body mass index (BMI), sex and baseline age. RESULTS: In most countries, more educated individuals performed better on both memory tests at baseline, compared to those less educated. However, education was not protective against faster decline, except for in Spain for both immediate and delayed recall (0.007 (SE=0.003) & 0.006 (SE=0.002), and Switzerland for immediate recall 0.006 (SE=0.003). Interestingly, highly educated Italian respondents had slightly faster declines in immediate recall (-0.006 (SE=0.003)). CONCLUSIONS: We found weak evidence of a protective effect of education on memory change in most European samples, although there was a positive association with memory performance at individuals' baseline assessment

The European Prevention of Alzheimer's Dementia (EPAD) Longitudinal Cohort Study: Baseline Data Release V500.0.

BACKGROUND: The European Prevention of Alzheimer's Dementia (EPAD) Programme is a pan-European project whose objective is to deliver a platform, adaptive, Phase 2 proof of concept (PoC) trial for the secondary prevention of Alzheimer's dementia. A component of this platform is the Longitudinal Cohort Study (LCS) which acts as a readiness cohort for the PoC Trial as well as generating data for disease modelling work in the preclinical and prodromal phases of Alzheimer's dementia. OBJECTIVES: The first data wave has been collected, quality checked, released and now available for analysis to answer numerous research questions. Here we describe the results from key variables in the EPAD LCS with the objective of using these results to compliment analyses of these data in the future. DESIGN: EPAD LCS is a cohort study whose primary objective is as a readiness cohort for the EPAD PoC Trial. As such recruitment is not capped at any particular number but will continue to facilitate delivery of the EPAD PoC Trial. Research Participants are seen annually (with an additional 6 month visit in the first year). SETTING: The EPAD Trial Delivery Network comprises currently 21 centres across Europe. PARTICIPANTS: Research participants are included if they are over 50 years old and do not have a diagnosis of dementia. MEASUREMENTS: All research participants undergo multiple assessments to fully characterise the biology of Alzheimer's disease and relate this to risk factors (both fixed and modifiable) and biomarker expression of disease through brain imaging, fluid samples (CSF, blood, urine and saliva), cognitive performance, functional abilities and neuropsychiatric symptomatology. RESULTS: V500.0 represents the first 500 research participants baselined into EPAD LCS. The mean age was 66.4 (SD=6.7) and 47.8% were male. The data was split for presentation into 4 groups: [1] CDR=0 and Amyloid + (preclinical AD), [2] CDR=0 and Amyloid -, [3] CDR=0.5 and Amyloid + (prodromal AD) and [4] CDR=0.5 and Amyloid -. CONCLUSIONS: The EPAD LCS is achieving its primary objective of trial readiness and the structured approach to data release as manifest by this first data release of V500.0 will assist researchers to describe and compare their findings as well as in systematic reviews and meta-analyses. It is anticipated given current recruitment rates that V1500.0 data release will take place in Autumn 2019. V500.1 (when the 1 year follow up is completed on the V500.0 (sub)cohort will be in Autumn 2019 also.IMI Fundin

Associations of body mass index and sarcopenia with screen-detected mild cognitive impairment in older adults in Colombia

Background and objective: More research is required to understand associations of body mass index (BMI) and sarcopenia with cognition, especially in Latin America. The objective of this study was to investigate associations of BMI and sarcopenia with mild cognitive impairment in Colombia. Design setting and participants: Data were from the National Survey of Health, Wellbeing and Aging in Colombia (SABE Colombia, in Spanish). Community-dwelling adults aged 60 years or older were invited to participate. Methods: Trained interviewers administered a shorter version of the mini-mental state examination and mild cognitive impairment was defined as a score of 12 or less out of 19. Body mass index was defined using standard cut-offs. Sarcopenia was defined as low grip strength or slow chair stands. Logistic regression models were adjusted for age, sex, height, education, income, civil status, smoking, and alcohol drinking. Results: The prevalence of mild cognitive impairment was 20% in 23,694 participants in SABE Colombia and 17% in 5,760 participants in the sub-sample in which sarcopenia was assessed. Overweight and obesity were associated with decreased risk of mild cognitive impairment and sarcopenia was associated with increased risk. Sarcopenia was a risk factor for mild cognitive impairment in those with normal BMI (adjusted model included 4,911 men and women). Compared with those with normal BMI and without sarcopenia, the odds ratio for mild cognitive impairment was 1.84 in those with normal BMI and sarcopenia (95% confidence interval: 1.25, 2.71). Sarcopenia was also a risk factor in those with obesity but did not present a greater risk than sarcopenia alone. Compared with those with normal BMI and without sarcopenia, the odds ratio was 1.62 in those with obesity and sarcopenia (95% confidence interval: 1.07, 2.48). Sarcopenia was not a risk factor for mild cognitive impairment in those with overweight. Similar results were observed when reference values from Colombia were used to set cut-offs for grip strength. Similar results were also observed in cross-validation models, which suggests the results are robust. Conclusion: This is the first study of the combined associations of sarcopenia and obesity with cognition in Colombia. The results suggest that sarcopenia is the major predictor of screen-detected mild cognitive impairment in older adults, not overweight or obesity