P1‐152: ACTIVATION OF INFLAMMATION IS ASSOCIATED WITH Aβ ACCUMULATION INDUCED BY CHRONIC SLEEP RESTRICTION IN RATS

Alzheimer's disease (AD) is the most common age-associated neurodegenerative disease featured by progressive learning and memory deficit, and Aβ 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 has found that chronic sleep restriction (CSR) caused cognitive impairment and Aβ accumulation in rats, but the underlining mechanism was unclear. In present study, we investigated the effects of inflammation on Aβ accumulation induced by CSR. Ten-month old Sprague-Dawley rats were used in this study, and rats in CSR groups were conducted by rolling drums. Inflammation biomarkers in brain and plasma were tested, and the correlation analysis were conducted. We found that CSR significantly increased the expression of interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), inducible nitric oxide synthase (iNOS) and nitric oxide (NO) in the brain, and the inflammation factors levels were positively correlated with the Aβ42 deposition. Additionally, the inflammation factors were correlated with BACE1, LRP-1 and RAGE levels in both the hippocampus and the prefrontal cortex. Furthermore, the plasma levels of IL-1β, TNF-α and NO were elevated after CSR, and the concentration of plasma inflammatory mediators was correlated with plasma levels of sLRP1 and sRAGE. These results suggested that the inflammation in brain and plasma may be involved in the CSR-induced Aβ accumulation.