In Context

The European Dementia Prevention Initiative

There is evidence of the role of vitamin D deficiency in cognitive decline. However, the results of studies regarding the relationship between the reduction of vitamin D concentrations and cognitive impairment are heterogeneous.

We aimed to answer the question of whether vitamin D deficiency is associated with cognitive decline in older adults.

In this cross-sectional study, the baseline data of the Birjand Longitudinal Aging Study (BLAS) were analyzed. Of 1420 participants in the BLAS, 1219 participants aged ≥60 y old were included in the present study. Serum concentrations of 25-hydroxyvitamin D [25(OH)D] were measured by the enzyme-linked immunosorbent assay method. The 6-item Cognitive Impairment Test (6-CIT), Mini-Mental State Examination (MMSE), Category Fluency Test (CFT), and Abbreviated Mental Test Score (AMTS) were used to assess cognitive function. Multiple logistic regression analysis, adjusted for potential confounders, was employed to estimate the association between cognitive function and 25(OH)D concentrations.

Among study participants, 905 (74.24%) had sufficient vitamin D concentrations (≥20 ng/ml), 209 (17.15%) had insufficient vitamin D concentrations (12–20 ng/ml), and 105 (8.61%) had vitamin D deficiency (<12 ng/ml). There was no significant correlation between serum 25(OH)D concentrations and scores of 6-CIT (P = 0.279), AMTS (P = 0.181), MMSE (P = 0.118), and CFT (P = 0.259). Also, the prevalence of cognitive impairment had no significant relationship with vitamin D status. Finally, in the multiple logistic regression analysis, there was no association between the insufficient or deficient concentrations of 25(OH)D and impaired cognitive function both before and after adjustment for various cofounders.

The present study found no significant association between vitamin D status and cognitive impairment.

The global population is aging, leading to an increasing burden of age-related neurodegenerative disease. Efforts to intervene against age-related dementias in older adults have generally proven ineffective. These failures suggest that a lifetime of brain aging may be difficult to reverse once widespread deterioration has occurred. To test interventions in younger populations, biomarkers of brain aging are needed that index subtle signs of accelerated brain deterioration that are part of the putative pathway to dementia. Here I review potential MRI-based biomarkers that could connect midlife brain aging to later life dementia. I survey the literature with three questions in mind, 1) Does the biomarker index age-related changes across the lifespan? 2) Does the biomarker index cognitive ability and cognitive decline? 3) Is the biomarker sensitive to known risk factors for dementia? I find that while there is preliminary support for some midlife MRI-based biomarkers for accelerated aging, the longitudinal research that would best answer these questions is still in its infancy and needs to be further developed. I conclude with suggestions for future research.

Interventions that have even quite modest effects at the individual level could drastically reduce the future burden of dementia associated with Alzheimer's disease at the population level. In the past three decades, both pharmacological and lifestyle interventions have been studied for the prevention of cognitive decline or dementia in randomised controlled trials of individuals mostly aged older than 50–55 years with or without risk factors for Alzheimer's disease. Several trials testing the effects of physical activity, cognitive training, or antihypertensive interventions showed some evidence of efficacy on a primary cognitive endpoint. However, most of these trials had short follow-up periods, and further evidence is needed to confirm effectiveness and establish the optimum design or dose of interventions and ideal target populations. Important innovations in ongoing trials include the development of multidomain interventions, and the use of biomarker or genetic inclusion criteria. Challenges include the use of adaptive trial designs, the development of standardised, sensitive outcome measures, and the need for interventions that can be implemented in resource-poor settings.

Although patients with type 2 diabetes are twice as likely to develop dementia as those without this disease, prediction of who has the highest future risk is difficult. We therefore created and validated a practical summary risk score that can be used to provide an estimate of the 10 year dementia risk for individuals with type 2 diabetes.

Using data from two longitudinal cohorts of patients with type 2 diabetes (aged ≥60 years) with 10 years of follow-up, we created (n=29 961) and validated (n=2413) the risk score. We built our prediction model by evaluating 45 candidate predictors using Cox proportional hazard models and developed a point system for the risk score based on the size of the predictor's β coefficient. Model prediction was tested by discrimination and calibration methods. Dementia risk per sum score was calculated with Kaplan-Meier estimates.

Microvascular disease, diabetic foot, cerebrovascular disease, cardiovascular disease, acute metabolic events, depression, age, and education were most strongly predictive of dementia and constituted the risk score (C statistic 0·736 for creation cohort and 0·746 for validation cohort). The dementia risk was 5·3% (95% CI 4·2–6·3) for the lowest score (–1) and 73·3% (64·8–81·8) for the highest (12–19) sum scores.

To the best of our knowledge, this is the first risk score for the prediction of 10 year dementia risk in patients with type 2 diabetes mellitus. The risk score can be used to increase vigilance for cognitive deterioration and for selection of high-risk patients for participation in clinical trials.

Kaiser Permanente Community Benefit, National Institute of Health, Utrecht University, ZonMw, and Fulbright.

Process-based cognitive trainings (PCTs) and novelty interventions are two traditional approaches aiming to prevent cognitive decline and dementia. However, both have their limitations. PCTs improve performance only in cognitive tests similar to the training tasks with inconsistent transfer effects on dissimilar tests. We argue that this learning specificity is due to a low training task variability. Novelty interventions are characterized by a high task variability but do not target specific processing demands affected in aging and dementia. To overcome the limitations of both approaches, we developed a process-based novelty intervention using a card and board game-based training approach. Here, we use highly variable tasks, which overlap in targeted processing demands (“overlapping variability” framework). Another nontraditional training approach combines cognitively with physically challenging tasks to induce multimechanistic effects, which might even interact positively. Initial results of both synergistic approaches indicate their potential to enhance broad cognitive abilities and prevent dementia.