Sajeev Gautam, Weuve Jennifer, Jackson John W, VanderWeele Tyler J, Bennett David A, Grodstein Francine, Blacker Deborah
From the aDepartment of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA; bDepartment of Epidemiology, Boston University School of Public Health, Boston, MA; cDepartment of Biostatistics, Harvard T.H. Chan School of Public Health, Boston, MA; dRush Alzheimer's Disease Center, Rush University Medical Center, Chicago, IL; eBrigham and Women's Hospital, Boston, MA; and fGerontology Research Unit, Department of Psychiatry, Massachusetts General Hospital, Boston, MA.
Epidemiology. 2016 Sep;27(5):732-42. doi: 10.1097/EDE.0000000000000513.
Engaging in late-life cognitive activity is often proposed as a strategy to delay or prevent Alzheimer's disease (AD) and other dementias. However, it is unclear to what extent the available evidence supports a causal effect of cognitive activity in dementia prevention.
We systematically searched PubMed and EMBASE through June 2014 to identify peer-reviewed epidemiologic studies of cognitive activity and incidence of AD or all-cause dementia. Eligible articles analyzed data from cohort or nested case-control studies, explicitly defined cognitive activity, evaluated participants for AD or all-cause dementia using clearly defined criteria, and provided effect estimates adjusted for at least age and sex. We describe methodologic issues and biases relevant to interpretation of these studies, and quantify the degree of bias due to confounding and reverse causation required to nullify typically observed associations.
We reviewed 12 studies involving 13,939 participants and 1,663 dementia cases, of which 565 were specifically evaluated as AD. Most studies found associations between late-life cognitive activity and lower AD and/or all-cause dementia incidence. Differences in cognitive activity operationalization across studies precluded meta-analysis of effect estimates. Our bias analysis indicated that the observed inverse associations are probably robust to unmeasured confounding, and likely only partially explained by reverse causation.
Our systematic review and bias analyses provide support for the hypothesis that late-life cognitive activity offers some reduction in AD and all-cause dementia risk. However, more data are needed to confirm this relationship and on the optimal type, duration, intensity, and timing of that activity.
参与晚年认知活动常被视为延缓或预防阿尔茨海默病(AD)及其他痴呆症的一种策略。然而,现有证据在多大程度上支持认知活动对预防痴呆症具有因果效应尚不清楚。
我们系统检索了截至2014年6月的PubMed和EMBASE数据库,以确定关于认知活动与AD或全因性痴呆发病率的同行评审流行病学研究。符合条件的文章分析了队列研究或巢式病例对照研究的数据,明确界定了认知活动,使用明确的标准对参与者进行AD或全因性痴呆评估,并提供了至少根据年龄和性别进行调整的效应估计值。我们描述了与这些研究的解释相关的方法学问题和偏差,并量化了由于混杂因素和反向因果关系导致的偏差程度,这些偏差会使通常观察到的关联无效。
我们回顾了12项研究,涉及13939名参与者和1663例痴呆症病例,其中565例被专门评估为AD。大多数研究发现晚年认知活动与较低的AD和/或全因性痴呆发病率之间存在关联。各研究在认知活动操作定义上的差异使得无法对效应估计值进行荟萃分析。我们的偏差分析表明,观察到的反向关联可能对未测量的混杂因素具有稳健性,并且可能仅部分由反向因果关系解释。
我们的系统评价和偏差分析支持这样一种假设,即晚年认知活动可在一定程度上降低AD和全因性痴呆的风险。然而,需要更多数据来证实这种关系以及该活动的最佳类型、持续时间、强度和时机。