Melatonin ameliorates A1-42-induced Alzheimer's cognitive deficits in mouse model

ObjectivesThe objective of this study was to evaluate whether melatonin could ameliorate cognitive function in A(1-42)-induced mouse model and its underlying mechanisms. MethodsSeries behaviour tests were performed to demonstrate the amelioration of cognitive function of the Alzheimer's disease (AD) mice induced by A(1-42). Additionally, enzyme-linked immunosorbent assay was applied to detect the expression of A(1-42), 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-3 and PP2A to further determine the mechanisms of melatonin on the expression of p-tau protein. Key findingsMelatonin significantly ameliorated the cognitive function and mitochondrial damage in AD mice, reduced the expression levels of GSK-3, caspase-3, A(1-42), BACE1, p-tau protein and increased the expressions of PP2A and Bcl-2. ConclusionFrom 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 A(1-42).