ArticleJournal of cellular and molecular medicine2021
Adiponectin improves amyloid-β 31-35-induced circadian rhythm disorder in mice.
Article in Journal of cellular and molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- Adiponectin modulates the diurnal hepatic transcriptome and energy metabolism in male mice.Endocrine connections · 2026Article
- Exploring bacterial metabolites in microbe-human host dialogue and their therapeutic potential in Alzheimer's diseases.Molecular diversity · 2025Article
- IL-17A Induces Circadian Disruptions Through the Epigenetic Repression of BMAL1 in Mice With Alzheimer's Disease.Journal of cellular and molecular medicine · 2025Article
- Association between circadian syndrome and the prevalence of kidney stones in overweight adults: a cross-sectional analysis of NHANES 2007-2018.BMC public health · 2023Article
- Importance of Bmal1 in Alzheimer's disease and associated aging-related diseases: Mechanisms and interventions.Aging cell · 2022Review
- Adiponectin improves amyloid-β 31-35-induced circadian rhythm disorder in mice.Journal of cellular and molecular medicine · 2021Article
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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.
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