Activation of Inflammation is Associated with Amyloid-β Accumulation Induced by Chronic Sleep Restriction in Rats

Published on Jan 1, 2020in Journal of Alzheimer's Disease3.909
· DOI :10.3233/JAD-191317
Peng Liu2
Estimated H-index: 2
(Xi'an Jiaotong University),
Beiyu Zhao4
Estimated H-index: 4
(Xi'an Jiaotong University)
+ 8 AuthorsQiumin Qu8
Estimated H-index: 8
(Xi'an Jiaotong University)
Alzheimer's disease (AD) is the most common age-associated neurodegenerative disease featured by progressive learning and memory deficit, and Abeta was identified as playing a key role in the process of AD and was theorized to be caused by the imbalance of production and clearance. Increasing evidence suggested an association between sleep deprivation and AD. Our recent study found that chronic sleep restriction (CSR) caused cognitive impairment and Abeta accumulation in rats, but the underlining mechanism was unclear. In the present study, we investigated the effects of inflammation on Abeta accumulation induced by CSR. We found that CSR significantly increased the expression of interleukin-1beta (IL-1beta), tumor necrosis factor-alpha (TNF-alpha), inducible nitric oxide synthase (iNOS), and nitric oxide (NO) in brain, and the inflammatory factors levels were positively correlated with Abeta42 deposition. Additionally, the inflammatory factors were correlated with BACE1, LRP-1, and RAGE levels in both the hippocampus and the prefrontal cortex. Furthermore, the plasma levels of IL-1beta, TNF-alpha, and NO were elevated after CSR, and the concentration of plasma inflammatory mediators were correlated with plasma levels of sLRP1 and sRAGE. These results suggested that the inflammation in brain and plasma might be involved in the CSR-induced Abeta accumulation.
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