Nucleosome assembly protein 1-like 5 alleviates Alzheimer's disease-like pathological characteristics in a cell model

• Published in: Frontiers in molecular neuroscience Vol. 15; p. 1034766
• Main Authors: Wang, Bingyan, Liu, Weiying, Sun, Fengxian
• Format: Journal Article
• Language: English
• Published: Switzerland Frontiers Media S.A 08.12.2022
• Subjects: Alzheimer’s disease; APP metabolism; GSK3B; Molecular Neuroscience; NAP1L5; neuroinflammation; Tau phosphorylation; Tau phosphorylation; GSK3B; Alzheimer’s disease; Wnt/β-catenin signaling pathway; neuroinflammation; APP metabolism; NAP1L5
• ISSN: 1662-5099; 1662-5099
• DOI: 10.3389/fnmol.2022.1034766

Alzheimer's disease (AD) remains one of the most common dementias of neurodegenerative disease-related diseases. Nucleosome assembly protein 1-like 5 (NAP1L5) belongs to the NAP1L protein family, which acts as a histone chaperone. However, the function and mechanism of NAP1L5 in AD are still unclear. Bioinformatics analysis, RT-qPCR, and Western blotting results showed that NAP1L5 was downregulated in the brain tissues of AD patients and a mouse cell model of AD. NAP1L5 overexpression alleviated (Amyloid-β precursor protein) APP metabolism and Tau phosphorylation. We further demonstrated that NAP1L5 regulated the AD-like pathological characteristics through the GSK3B/Wnt/β-Catenin signaling pathway. Moreover, we showed that the Wnt/β-Catenin signaling pathway, regulated by NAP1L5, was mediated by AQP1-mediated mechanism in N2a-APP695sw cell. In sum, these results suggested that NAP1L5 overexpression has neuroprotective effects and might act as potential biomarker and target for the diagnosis and treatment of AD.