Background Dementia cases continues to grow in the era of ageing population, with its number approaching 50 million. Accumulating evidence has shown that high blood pressure increases the risk of dementia and cognitive decline. In recent decades, some studies demonstrate that blood pressure variability (BPV) may contribute to cognitive decline and incident dementia independent of the blood pressure level. However, due to the inconsistence of statistical results and clinical methodology, the magnitude of this relationship remains ambiguous. A clear understanding of the role of BPV in dementia may shed light to etiology and early prevention of dementia. This study aims to assess the association between BPV with incident dementia and cognitive impairment. Method We searched MEDLINE, Embase, PsycINFO, CINAHL and Web of Science from December 2020 for articles describing trials, retrospective and prospective cohort studies in adults that assessed the association of long‐term BPV (measured through clinic blood pressure monitoring) with incident dementia and cognitive impairment. 5681 papers were identified and eventually 12 articles with full text and 3 abstracts with enough information were included in the quantitative analysis. Of these 15 studies, 2 articles report both dementia and cognitive decline or dysfunction as outcomes, while 5 studies report dementia as an outcome and 8 studies report cognitive decline or dysfunction. Result Hazard Ratio and linear regression coefficient were converted to a standardized one. We found that increased long‐term variability in systolic blood pressure was associated with higher risk of all‐cause dementia [pooled standardized HR of 1.1 (95%CI, 1.01, 1.19)]. Compared to people in lower BPV group, people in higher BPV group was 1.17 times more likely to develop dementia [pooled HR 1.17 (95%CI,1.12, 1.22)]. Cognitive decline was associated with higher SBPV [pooled linear coefficient for MMSE score is ‐0.11(95%CI, ‐0.17, ‐0.05)],which means MMSE score decreases by 0.11 per SD increase in SBPV. Conclusion Our findings suggested that higher long‐term blood pressure variability increases both the risk for incident dementia and cognitive decline.
Background: Dementia remains a global burden in aged populations and its contributing factors are still poorly known. While the lack of sleep has been proposed as a risk factor for dementia, evidence has emerged that excessive sleep might also be associated with increased risk for dementia. The present systematic review and metaanalysis then aims to quantitatively clarify the correlation between dementia and sleep duration using a novel approach.Method: Literature databases including PubMed and Embase were searched for studies reporting statistics on the proportion of participants with dementia or mild cognitive impairment (MCI) as well as the corresponding sleep duration. Unlike existing methods that measure odds ratios and relative ratios of developing dementia, the data were used to form a beta distribution that shows the likelihood of developing dementia / MCI given the sleep duration. Result:The search identified a total of 6,522 articles, of these 10 studies involving 31510 participants in 7 countries were eligible for inclusion. The follow-up time of these studies varied between 1 to 14 years. The relationship between dementia / MCI was U-shaped. The distribution was asymmetrical with the implication that excessive sleep was associated with higher risk of dementia / MCI, compared with lack of sleep.In addition, higher risk of dementia rather than MCI was associated with sleep duration below 5 hours or above 9 hours. Conclusion:The asymmetry of the distribution suggests the difference in the pathogenesis of dementia between the lack of sleep and excessive sleep. Coupled with existing findings that excessive sleep does not lead to the deposition of β-amyloid, it is suggested that excessive sleep directly damages synapses in the absence of β-amyloid accumulation. While there is still no plausible physiologic explanation for how excessive sleep and dementia is mediated, some have argued that excessive sleep could elevate the level of proinflammatory cytokine that has been suggested to reduce synapses.
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