Revision of the apolipoprotein E compensatory mechanism recruitment hypothesis

被引：122

作者：

Han, S. Duke ^{[1
,2
,3
]}

Bondi, Mark W. ^{[4
,5
]}

机构：

[1] Loyola Univ, Dept Psychol, Chicago, IL 60626 USA

[2] Loyola Univ, Ctr Med, Dept Neurol, Maywood, IL 60153 USA

[3] Loyola Univ, Ctr Med, Inst Neurosci, Maywood, IL 60153 USA

[4] Univ Calif San Diego, Dept Psychiat, San Diego, CA 92103 USA

[5] VA San Diego Healthcare Syst, Psychol Serv, San Diego, CA USA

来源：

ALZHEIMERS & DEMENTIA | 2008年 / 4卷 / 04期

关键词：

apolipoprotein E; compensation; fMRI; neuropsychology; executive functions; memory;

D O I：

10.1016/j.jalz.2008.02.006

中图分类号：

R74 [神经病学与精神病学];

学科分类号：

摘要：

The association between the apolipoprotein E epsilon 4 allele and Alzheimer's disease (AD) is well-established. Functional neuroimaging research has supported a compensatory mechanism recruitment hypothesis whereby nondemented epsilon 4 participants use additional cognitive resources to buffer against episodic memory declines in older age, a mechanism that is presumably associated with encroaching disease. However, recent studies have implicated a beneficial effect associated with the epsilon 4 allele early in the life span. These studies suggest a revised hypothesis whereby epsilon 4 persons perform better on cognitive measures early in the life span and then show greater recruitment of brain regions during performance to compensate for declines in older age caused by preclinical AD. (C) 2008 The Alzheimer's Association. All rights reserved.

引用

页码：251 / 254

页数：4

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