Sleep: A Novel Mechanistic Pathway, Biomarker, and Treatment Target in the Pathology of Alzheimer's Disease?

被引:294
作者
Mander, Bryce A. [1 ]
Winer, Joseph R. [1 ]
Jagust, William J. [2 ,3 ]
Walker, Matthew P. [1 ,2 ]
机构
[1] Univ Calif Berkeley, Sleep & Neuroimaging Lab, Berkeley, CA 94720 USA
[2] Univ Calif Berkeley, Helen Wills Neurosci Inst, Berkeley, CA 94720 USA
[3] Lawrence Berkeley Natl Lab, Mol Biophys & Bioimaging Div, Berkeley, CA 94720 USA
基金
美国国家卫生研究院;
关键词
DIRECT-CURRENT STIMULATION; MILD COGNITIVE IMPAIRMENT; DEPENDENT MEMORY CONSOLIDATION; SLOW-WAVE SLEEP; APOLIPOPROTEIN-E EPSILON-4; EYE-MOVEMENT SLEEP; OLDER-ADULTS; ELDERLY SUBJECTS; IN-VIVO; A-BETA;
D O I
10.1016/j.tins.2016.05.002
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Sleep disruption appears to be a core component of Alzheimer's disease (AD) and its pathophysiology. Signature abnormalities of sleep emerge before clinical onset of AD. Moreover, insufficient sleep facilitates accumulation of amyloid-p (Am, potentially triggering earlier cognitive decline and conversion to AD. Building on such findings, this review has four goals: evaluating (i) associations and plausible mechanisms linking non-rapid-eye-movement (NREM) sleep disruption, AD, and AD; (ii) a role for NREM sleep disruption as a novel factor linking cortical AD to impaired hippocampus-dependent memory consolidation; (iii) the potential diagnostic utility of NREM sleep disruption as a new biomarker of AD; and (iv) the possibility of sleep as a new treatment target in aging, affording preventative and therapeutic benefits.
引用
收藏
页码:552 / 566
页数:15
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