Adiponectin improves amyloid‐β 31‐35‐induced circadian rhythm disorder in mice

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.

Importance of Bmal1 in Alzheimer's disease and associated aging‐related diseases: Mechanisms and interventions

“…Adiponectin, an adipocyte-derived hormone, ameliorates the aberrant expression of the Bmal1 mRNA/protein induced by Aβ31-35 via inhibition of GSK3β activity, and exogenous administration of adiponectin may be a promising treatment for AD (Yuan et al, 2021).…”

“…Another study found that TRF was related to increased Bmal1 mRNA levels in the liver and improved metabolic health (Regmi et al, 2021 ). Adiponectin, an adipocyte‐derived hormone, ameliorates the aberrant expression of the Bmal1 mRNA/protein induced by Aβ31‐35 via inhibition of GSK3β activity, and exogenous administration of adiponectin may be a promising treatment for AD (Yuan et al, 2021 ). NAD+ deficiency in diverse tissues with age contributes to the progress of multiple age‐related diseases such as T2DM, AD, vascular dysfunction (de Picciotto et al, 2016 ), and cerebral ischemia.…”