Chronic Sleep Restriction Induces Cognitive Deficits and Cortical Beta‐Amyloid Deposition in Mice via <scp>BACE</scp>1‐Antisense Activation

Abstract

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.