Adiponectin improves amyloid‐β 31‐35‐induced circadian rhythm disorder in mice. Issue 20 (15th September 2021)

• Record Type: Journal Article
• Authors: Yuan, Yuan; Li, Chen; Guo, Shuai; Sun, Cong; Ning, Na; Hao, Haihu; Wang, Li; Bian, Yunfei; Liu, Huirong; Wang, Xiaohui
• Is Part Of: Journal of cellular and molecular medicine. Volume 25:Issue 20(2021)
• Page Start: 9851
• Page End: 9862
• Publication Date: 2021-09-15
• Subjects: adiponectin -- Alzheimer's disease -- Aβ31‐35 -- Bmal1 -- GSK3β; Cytology; Medicine; Molecular Biology; Cytologie -- Périodiques; Médecine -- Périodiques; Biologie moléculaire -- Périodiques; Cytology -- Periodicals; Medicine -- Periodicals; Molecular biology -- Periodicals; 611.01805
• DOI: 10.1111/jcmm.16932
• Languages: English
• ISSNs: 1582-1838

Abstract

Abstract: Adiponectin is an adipocyte‐derived hormone, which is closely associated with the development of Alzheimer's disease (AD) and has potential preventive and therapeutic significance. In the present study, we explored the relationship between adiponectin and circadian rhythm disorder in AD, the effect of adiponectin on the abnormal expression of Bmal1 mRNA/protein induced by amyloid‐β protein 31‐35 (Aβ31‐35), and the underlying mechanism of action. We found that adiponectin‐knockout mice exhibited amyloid‐β deposition, circadian rhythm disorders and abnormal expression of Bmal1. Adiponectin ameliorated the abnormal expression of the Bmal1 mRNA/protein caused by Aβ31‐35 by inhibiting the activity of glycogen synthase kinase 3β (GSK3β). These results suggest that adiponectin deficiency could induce circadian rhythm disorders and abnormal expression of the Bmal1 mRNA/protein, whilst exogenous administration of adiponectin may improve Aβ31‐35‐induced abnormal expression of Bmal1 by inhibiting the activity of GSK3β, thus providing a novel idea for the treatment of AD.