Chronic Sleep Restriction Induces Cognitive Deficits and Cortical Beta-Amyloid Deposition in Mice via BACE1-Antisense Activation.

CONCLUSIONS: This study shows that a CSR accelerates AD pathogenesis in wild-type mice. An upregulation of the BACE1 pathway appears to participate in both cortical Aβ plaque deposition and memory impairment caused by CSR. BACE1-AS is likely activated to initiate a cascade of events that lead to AD pathogenesis. Our study provides, therefore, a molecular mechanism that links CSR to sporadic AD.
PMID: 28145081 [PubMed - as supplied by publisher]

Source: CNS Neuroscience and Therapeutics - January 31, 2017 Category: Neuroscience Authors: Zhao HY, Wu HJ, He JL, Zhuang JH, Liu ZY, Huang LQ, Zhao ZX Tags: CNS Neurosci Ther Source Type: research