Chronic sleep fragmentation shares similar pathogenesis with neurodegenerative diseases: Endosome‐autophagosome‐lysosome pathway dysfunction and microglia‐mediated neuroinflammation

• DOI: 10.1111/cns.13218
• Publication Date: 2019-09-24T10:33:29Z
• Authors: Yi Xie; Li Ba; Min Wang; Sai‐Yue Deng; Si‐Miao Chen; Li‐Fang Huang; Min Zhang; Wei Wang; Feng‐Fei Ding
• Keywords: Pathogenesis; Autophagosome; Fragmentation

Insufficient sleep has been found to result in varying degrees of cognitive impairment and emotional changes. Sleep was reported probably responsible for cleaning metabolic wastes brain by increasing extracellular bulk flow. Herein, we propose that chronic insufficiency young adult wild-type mice is also linked with dysfunction intracellular protein degradation pathways microglia-mediated neuroinflammation, which are potentially important mechanisms the initiation neurodegeneration.We applied fragmentation (CSF) model induce mice. After 2 months CSF, function, amyloid-β accumulation, endosome-autophagosome-lysosome pathway, microglia activation were evaluated.Following spatial learning memory, aggravated anxiety-like behavior identified behavioral experiments. Increased accumulation observed cortex hippocampus. Mechanistically, CSF could significantly enhance expression Rab5 (early endosome marker), Rab7 (late as well LC3B (autophagosome autophagy-positive regulatory factors detected immunofluorescent staining Western blot. In addition, evident enhanced CD68, CD16/32, CD206 levels after treatment.Chronic initiate pathogenetic processes similar early stage neurodegeneration, including pathway neuroinflammation. Our findings further strengthen link between neurodegeneration even if lack genetic predisposition.