Hippocampal atrophy and memory dysfunction associated with physical inactivity in community-dwelling elderly subjects: The Sefuri study.
Hippocampal atrophy and memory dysfunction associated with physical inactivity in community-dwelling elderly subjects: The Sefuri study.
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DOI：
10.1002/brb3.620
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发表时间：
2017-02
影响因子：
3.1
通讯作者：
Yao H
中科院分区：
文献类型：
--
作者：
Hashimoto M;Araki Y;Takashima Y;Nogami K;Uchino A;Yuzuriha T;Yao H
缺乏运动是海马萎缩和阿尔茨海默病可改变的危险因素之一。我们使用结构方程模型（SEM）研究了身体活动、海马萎缩和记忆之间的关系。我们研究了213名居住在社区的老年受试者（99名男性和114名女性，平均年龄为68.9岁），他们没有痴呆或临床明显的抑郁症。所有参与者都进行了迷你精神状态测试（MMSE）和Rivermead行为记忆测试（RBMT）。通过结构化问卷对身体活动进行评估。我们使用一个免费的软件程序-基于统计参数映射8和通过指数李代数的微分形态解剖配准的基于体素的阿尔茨海默病特定区域分析系统（VSRAD）来评估海马萎缩程度（z - score -下文简称为ZAdvance）。常规磁共振成像表现如下：无症状性脑梗死24例（11.3%）；深部白质病变，72例（33.8%）；心室周围高信号，n = 35 (16.4%)；脑微出血14例（6.6%）。基于扫描电镜的路径分析表明，从休闲活动到海马萎缩的直接路径(β =−。18, p < 0.01)和海马萎缩到记忆功能障碍（RBMT） (β =−。20例，p < 0.01)，差异均有统计学意义。从“海马”灰质体积到RBMT和MMSE的直接路径高度显著，而从“全脑”灰质体积到RBMT和MMSE的直接路径不显著。所提出的扫描电镜模型对数据拟合得相当好。基于目前的扫描电镜分析，我们发现海马萎缩与年龄和闲暇时间缺乏体育活动有关，海马萎缩似乎会导致记忆功能障碍，尽管我们无法从目前的观察性研究中推断海马萎缩与记忆功能障碍之间的因果关系或时间联系。
Physical inactivity is one of the modifiable risk factors for hippocampal atrophy and Alzheimer's disease. We investigated the relationship between physical activity, hippocampal atrophy, and memory using structural equation modeling (SEM). We examined 213 community‐dwelling elderly subjects (99 men and 114 women with a mean age of 68.9 years) without dementia or clinically apparent depression. All participants underwent Mini‐Mental State Examination (MMSE) and Rivermead Behavioral Memory Test (RBMT). Physical activities were assessed with a structured questionnaire. We evaluated the degree of hippocampal atrophy (z‐score—referred to as ZAdvance hereafter), using a free software program—the voxel‐based specific regional analysis system for Alzheimer's disease (VSRAD) based on statistical parametric mapping 8 plus Diffeomorphic Anatomical Registration Through an Exponentiated Lie algebra. Routine magnetic resonance imaging findings were as follows: silent brain infarction, n = 24 (11.3%); deep white matter lesions, n = 72 (33.8%); periventricular hyperintensities, n = 35 (16.4%); and cerebral microbleeds, n = 14 (6.6%). Path analysis based on SEM indicated that the direct paths from leisure‐time activity to hippocampal atrophy (β = −.18, p < .01) and from hippocampal atrophy to memory dysfunction (RBMT) (β = −.20, p < .01) were significant. Direct paths from “hippocampus” gray matter volume to RBMT and MMSE were highly significant, while direct paths from “whole brain” gray matter volume to RBMT and MMSE were not significant. The presented SEM model fit the data reasonably well. Based on the present SEM analysis, we found that hippocampal atrophy was associated with age and leisure‐time physical inactivity, and hippocampal atrophy appeared to cause memory dysfunction, although we are unable to infer a causal or temporal association between hippocampal atrophy and memory dysfunction from the present observational study.