OBJECTIVE To investigate whether a healthy lifestyle is associated with lower risk of dementia regardless of genetic risk. DESIGN, SETTING, AND PARTICIPANTS A retrospective cohort study that included adults of European ancestry aged at least 60 years without cognitive impairment or dementia at baseline. Participants joined the UK Biobank study from 2006 to 2010 and were followed up until 2016 or 2017. EXPOSURES A polygenic risk score for dementia with low (lowest quintile), intermediate (quintiles 2 to 4), and high (highest quintile) risk categories and a weighted healthy lifestyle score, including no current smoking, regular physical activity, healthy diet, and moderate alcohol consumption, categorized into favorable, intermediate, and unfavorable lifestyles. MAIN OUTCOMES AND MEASURES Incident all-cause dementia, ascertained through hospital inpatient and death records. RESULTS A total of 196 383 individuals (mean [SD] age, 64.1 [2.9] years; 52.7% were women) were followed up for 1 545 433 person-years (median [interquartile range] follow-up, 8.0 [7.4-8.6] years). Overall, 68.1% of participants followed a favorable lifestyle, 23.6% followed an intermediate lifestyle, and 8.2% followed an unfavorable lifestyle. Twenty percent had high polygenic risk scores, 60% had intermediate risk scores, and 20% had low risk scores. Of the participants with high genetic risk, 1.23% (95% CI, 1.13%-1.35%) developed dementia compared with 0.63% (95% CI, 0.56%-0.71%) of the participants with low genetic risk (adjusted hazard ratio, 1.91 [95% CI, 1.64-2.23]). Of the participants with a high genetic risk and unfavorable lifestyle, 1.78% (95% CI, 1.38%-2.28%) developed dementia compared with 0.56% (95% CI, 0.48%-0.66%) of participants with low genetic risk and favorable lifestyle (hazard ratio, 2.83 [95% CI, 2.09-3.83]). There was no significant interaction between genetic risk and lifestyle factors (P = .99). Among participants with high genetic risk, 1.13% (95% CI, 1.01%-1.26%) of those with a favorable lifestyle developed dementia compared with 1.78% (95% CI, 1.38%-2.28%) with an unfavorable lifestyle (hazard ratio, 0.68 [95% CI, 0.51-0.90]). CONCLUSIONS AND RELEVANCE Among older adults without cognitive impairment or dementia, both an unfavorable lifestyle and high genetic risk were significantly associated with higher dementia risk. A favorable lifestyle was associated with a lower dementia risk among participants with high genetic risk.

Published studies suggest that greater adherence to Mediterranean diet is associated with slower cognitive decline and lower risk of developing Alzheimer disease. Further studies would be useful to clarify the association with mild cognitive impairment and vascular dementia. Long-term randomized controlled trials promoting a Mediterranean diet may help establish whether improved adherence helps to prevent or delay the onset of Alzheimer disease and dementia.

INTRODUCTION: Stroke is an established risk factor for all-cause dementia, though meta-analyses are needed to quantify this risk. METHODS: We searched Medline, PsycINFO and Embase for studies assessing prevalent or incident stroke versus a no-stroke comparison group and the risk of all-cause dementia. Random effects meta-analysis was used to pool adjusted estimates across studies and meta-regression was used to investigate potential effect modifiers. RESULTS: We identified 36 studies of prevalent stroke (1.9 million participants) and 12 studies of incident stroke (1.3 million participants). For prevalent stroke, the pooled hazard ratio for all-cause dementia was 1.69 (95% CI: 1.49–1.92; p<0.00001; I2 = 87%). For incident stroke, the pooled risk ratio was 2.18 (95% CI: 1.90–2.50; p<0.00001; I2 = 88%). Study characteristics did not modify these associations, with the exception of sex which explained 50.2% of between-study heterogeneity for prevalent stroke. DISCUSSION: Stroke is a strong, independent, and potentially modifiable risk factor for all-cause dementia.

BackgroundThe need to better understand implementing evidence-informed dementia care has been recognised in multiple priority-setting partnerships. The aim of this scoping review was to give an overview of the state of the evidence on implementation and dissemination of dementia care, and create a systematic evidence map.MethodsWe sought studies that addressed dissemination and implementation strategies or described barriers and facilitators to implementation across dementia stages and care settings. Twelve databases were searched from inception to October 2015 followed by forward citation and grey literature searches. Quantitative studies with a comparative research design and qualitative studies with recognised methods of data collection were included. Titles, abstracts and full texts were screened independently by two reviewers with discrepancies resolved by a third where necessary. Data extraction was performed by one reviewer and checked by a second. Strategies were mapped according to the ERIC compilation.ResultsEighty-eight studies were included (30 quantitative, 34 qualitative and 24 mixed-methods studies). Approximately 60% of studies reported implementation strategies to improve practice: training and education of professionals (94%), promotion of stakeholder interrelationships (69%) and evaluative strategies (46%) were common; financial strategies were rare (15%). Nearly 70% of studies reported barriers or facilitators of care practices primarily within residential care settings. Organisational factors, including time constraints and increased workload, were recurrent barriers, whereas leadership and managerial support were often reported to promote implementation. Less is known about implementation activities in primary care and hospital settings, or the views and experiences of people with dementia and their family caregivers.ConclusionThis scoping review and mapping of the evidence reveals a paucity of robust evidence to inform the successful dissemination and implementation of evidence-based dementia care. Further exploration of the most appropriate methods to evaluate and report initiatives to bring about change and of the effectiveness of implementation strategies is necessary if we are to make changes in practice that improve dementia care.Electronic supplementary materialThe online version of this article (doi:10.1186/s12877-017-0528-y) contains supplementary material, which is available to authorized users.

BackgroundMetabolic factors are increasingly recognized to play an important role in the pathogenesis of Alzheimer’s disease and dementia. Abnormal parathyroid hormone (PTH) levels play a role in neuronal calcium dysregulation, hypoperfusion and disrupted neuronal signaling. Some studies support a significant link between PTH levels and dementia whereas others do not.MethodsWe conducted a systematic review through January 2014 to evaluate the association between PTH and parathyroid conditions, cognitive function and dementia. Eleven electronic databases and citation indexes were searched including Medline, Embase and the Cochrane Library. Hand searches of selected journals, reference lists of primary studies and reviews were also conducted along with websites of key organizations. Two reviewers independently screened titles and abstracts of identified studies. Data extraction and study quality were performed by one and checked by a second reviewer using predefined criteria. A narrative synthesis was performed due to the heterogeneity of included studies.ResultsThe twenty-seven studies identified were of low and moderate quality, and challenging to synthesize due to inadequate reporting. Findings from six observational studies were mixed but suggest a link between higher serum PTH levels and increased odds of poor cognition or dementia. Two case-control studies of hypoparathyroidism provide limited evidence for a link with poorer cognitive function. Thirteen pre-post surgery studies for primary hyperparathyroidism show mixed evidence for improvements in memory though limited agreement in other cognitive domains. There was some degree of cognitive impairment and improvement postoperatively in observational studies of secondary hyperparathyroidism but no evident pattern of associations with specific cognitive domains.ConclusionsMixed evidence offers weak support for a link between PTH, cognition and dementia due to the paucity of high quality research in this area.