Background Physical exercise is seen as a promising intervention to prevent or delay cognitive decline in individuals aged 50 years and older, yet the evidence from reviews is not conclusive. Objectives To determine if physical exercise is effective in improving cognitive function in this population. Design Systematic review with multilevel meta-analysis. Data sources Electronic databases Medline (PubMed), EMBASE (Scopus), PsychINFO and CENTRAL (Cochrane) from inception to November 2016. Eligibility criteria Randomised controlled trials of physical exercise interventions in community-dwelling adults older than 50 years, with an outcome measure of cognitive function. Results The search returned 12 820 records, of which 39 studies were included in the systematic review. Analysis of 333 dependent effect sizes from 36 studies showed that physical exercise improved cognitive function (0.29; 95% CI 0.17 to 0.41; p<0.01). Interventions of aerobic exercise, resistance training, multicomponent training and tai chi, all had significant point estimates. When exercise prescription was examined, a duration of 45–60 min per session and at least moderate intensity, were associated with benefits to cognition. The results of the meta-analysis were consistent and independent of the cognitive domain tested or the cognitive status of the participants. Conclusions Physical exercise improved cognitive function in the over 50s, regardless of the cognitive status of participants. To improve cognitive function, this meta-analysis provides clinicians with evidence to recommend that patients obtain both aerobic and resistance exercise of at least moderate intensity on as many days of the week as feasible, in line with current exercise guidelines.

Summary: The relationship between body mass index (BMI) (in midlife and late‐life) and dementia was investigated in meta‐analyses of 16 articles reporting on 15 prospective studies. Follow‐ups ranged from 3.2 to 36.0 years. Meta‐analyses were conducted on samples including 25 624 participants evaluated for Alzheimer's disease (AD), 15 435 participants evaluated for vascular dementia (VaD) and 30 470 followed for any type of dementia (Any Dementia). Low BMI in midlife was associated with 1.96 [95% confidence interval (CI): 1.32, 2.92] times the risk of developing AD. The pooled relative risks for AD, VaD and Any Dementia for overweight BMI in midlife compared with normal BMI were 1.35 (95% CI:1.19, 1.54), 1.33 (95% CI: 1.02, 1.75) and 1.26 (95% CI: 1.10, 1.44), respectively. The pooled relative risks of AD and Any Dementia for obese BMI in midlife compared to normal BMI were 2.04 (95% CI: 1.59, 2.62) and 1.64 (95% CI: 1.34, 2.00), respectively. Continuous BMI in late‐life was not associated with dementia. Small numbers of studies included in pooled analyses reduce generalizability of findings, and emphasize the need for publication of additional findings. We conclude that underweight, overweight and obesity in midlife increase dementia risk. Further research evaluating late‐life BMI and dementia is required.

Changes in criteria and differences in populations studied and methodology have produced a wide range of prevalence estimates for mild cognitive impairment (MCI). Uniform criteria were applied to harmonized data from 11 studies from USA, Europe, Asia and Australia, and MCI prevalence estimates determined using three separate definitions of cognitive impairment. The published range of MCI prevalence estimates was 5.0%–36.7%. This was reduced with all cognitive impairment definitions: performance in the bottom 6.681% (3.2%–10.8%); Clinical Dementia Rating of 0.5 (1.8%–14.9%); Mini-Mental State Examination score of 24–27 (2.1%–20.7%). Prevalences using the first definition were 5.9% overall, and increased with age (P < .001) but were unaffected by sex or the main races/ethnicities investigated (Whites and Chinese). Not completing high school increased the likelihood of MCI (P ≤ .01). Applying uniform criteria to harmonized data greatly reduced the variation in MCI prevalence internationally.

Recent meta-analyses confirm a relationship between diet quality and both depression and cognitive health in adults. While the biological pathways that underpin these relationships are likely multitudinous, extensive evidence from animal studies points to the involvement of the hippocampus. The aim of this study was to examine the association between dietary patterns and hippocampal volume in humans, and to assess whether diet was associated with differential rates of hippocampal atrophy over time. Data were drawn from the Personality and Total Health Through Life Study and focused on a subsample of the cohort (n = 255) who were aged 60–64 years at baseline in 2001, completed a food frequency questionnaire, and underwent two magnetic resonance imaging scans approximately 4 years apart. Longitudinal generalized estimating equation linear regression models were used to assess the association between dietary factors and left and right hippocampal volumes over time. Every one standard deviation increase in healthy “prudent” dietary pattern was associated with a 45.7 mm3 (standard error 22.9 mm3) larger left hippocampal volume, while higher consumption of an unhealthy “Western” dietary pattern was (independently) associated with a 52.6 mm3 (SE 26.6 mm3) smaller left hippocampal volume. These relationships were independent of covariates including age, gender, education, labour-force status, depressive symptoms and medication, physical activity, smoking, hypertension and diabetes. While hippocampal volume declined over time, there was no evidence that dietary patterns influenced this decline. No relationships were observed between dietary patterns and right hippocampal volume. Lower intakes of nutrient-dense foods and higher intakes of unhealthy foods are each independently associated with smaller left hippocampal volume. To our knowledge, this is the first human study to demonstrate associations between diet and hippocampal volume concordant with data previously observed in animal models.