Abstract
Objectives:
The objective of this study was to evaluate whether melatonin could ameliorate cognitive function in Aβ1-42 -induced mouse model and its underlying mechanisms.
Methods:
Series behaviour tests were performed to demonstrate the amelioration of cognitive function of the Alzheimer's disease (AD) mice induced by Aβ1-42 . Additionally, enzyme-linked immunosorbent assay was applied to detect the expression of Aβ1-42 , BACE1 and p-tau protein in the brain of the AD mice. JC-1 was performed to investigate the role in alleviating mitochondrial damage by melatonin in vitro. Western blot was used to detect the expression of melatonin on apoptosis-related factors caspase-3 and Bcl-2, as well as the expressions of GSK-3β and PP2A to further determine the mechanisms of melatonin on the expression of p-tau protein.
Key findings:
Melatonin significantly ameliorated the cognitive function and mitochondrial damage in AD mice, reduced the expression levels of GSK-3β, caspase-3, Aβ1-42 , BACE1, p-tau protein and increased the expressions of PP2A and Bcl-2.
Conclusion:
From the overall results, we concluded that melatonin alleviated the mitochondrial damage effectively and decreased the expressions of the p-tau and some key proteins of apoptosis, leading to the improvement of cognitive function of the mice induced by Aβ1-42 .
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