Oxidative stress is associated with Aβ accumulation in chronic sleep deprivation model

• Published in: Brain research 2024-04, Vol.1829, p.148776-148776, Article 148776
• Main Authors: Beiyu, Zhao, Rong, Zhou, Yi, Zhao, Shan, Wei, Peng, Liu, Meng, Wei, Wei, Peng, Ye, Yuan, Qiumin, Qu
• Format: Article
• Language: English
• Subjects: Alzheimer Disease - pathology; Alzheimer’s disease; Amyloid beta-Peptides - metabolism; Amyloid Precursor Protein Secretases - metabolism; Amyloid-β; Animals; Aspartic Acid Endopeptidases - metabolism; Chronic sleep deprivation; Glycation End Products, Advanced - metabolism; Oxidative Stress; Rats; Reactive Oxygen Species; Sleep Deprivation; Superoxide Dismutase
• ISSN: 0006-8993; 1872-6240
• DOI: 10.1016/j.brainres.2024.148776

[Display omitted] •Brain and peripheral oxidation was activated after chronic sleep deprivation in rats.•Oxidation was correlated with Aβ production in CSD-rats.•Oxidation was correlated with brain and plasma clearance of Aβ in CSD-rats. Amyloid-β (Aβ) accumulation is the main pathological change in Alzheimer's disease (AD), which results from the imbalance of production and clearance of Aβ in the brain. Our previous study found that chronic sleep deprivation (CSD) led to the deposition of Aβ in the brain by disrupting the balance of Aβ production and clearance, but the specific mechanism was not clear. In the present study, we investigated the effects of oxidative stress on Aβ accumulation in CSD rats. We found that the levels of reactive oxygen species (ROS) and malondialdehyde (MDA) significantly increased after CSD, while superoxide dismutase (SOD) decreased in the brain. Furthermore, the serum ROS was elevated and SOD declined after CSD. The levels of oxidative stress in the brain were significantly correlated with β-site APP-cleaving enzyme 1 (BACE1), low-density lipoprotein receptor-related protein-1 (LRP1), and receptor of advanced glycation end products (RAGE) levels in hippocampus and prefrontal lobe, and the concentration of serum oxidative mediators were strongly correlated with plasma levels of soluble LRP1 (sLRP1) and soluble RAGE (sRAGE). These results suggested that the oxidative stress in the brain and serum may involved in the CSD-induced Aβ accumulation. The underlying mechanism may be associated with disrupting the balance of Aβ production and clearance.