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

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• 作者：Bryce A. Mander¹ ; ^{bamander@berkeley.edu" class="auth_mail" title="E-mail the corresponding author} ; Joseph R. Winer¹ ; William J. Jagust² ; ³ ; Matthew P. Walker¹ ; ² ; ^{mpwalker@berkeley.edu" class="auth_mail" title="E-mail the corresponding author}
• 关键词：sleep ; Alzheimer's disease ; amyloid-β ; aging ; cognitive decline
• 刊名：Trends in Neurosciences
• 出版年：2016
• 出版时间：August 2016
• 年：2016
• 卷：39
• 期：8
• 页码：552-566
• 全文大小：2345 K

文摘

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-β (Aβ), 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, Aβ, and AD; (ii) a role for NREM sleep disruption as a novel factor linking cortical Aβ 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.