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Melatonin ameliorates Aβ1-42 -induced Alzheimer's cognitive deficits in mouse model
Yu-Hang Gong1, Nan Hua1, Xuan Zang1
1Department of Pharmacology, China Pharmaceutical University, Nanjing, China.
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 .
Insights
Melatonin improved cognitive function in Alzheimer's disease (AD) mice by reducing amyloid-beta (Aβ) and tau pathology, and alleviating mitochondrial damage.
Area of Science:
- Neuroscience
- Biochemistry
- Pharmacology
Background:
- Alzheimer's disease (AD) is characterized by amyloid-beta (Aβ) plaques and tau pathology.
- Cognitive decline and mitochondrial dysfunction are key features of AD.
Purpose of the Study:
- To investigate melatonin's efficacy in ameliorating cognitive deficits in an Aβ₁-42-induced AD mouse model.
- To elucidate the underlying mechanisms, including effects on Aβ, tau, apoptosis, and mitochondrial function.
Main Methods:
- Behavioral tests assessed cognitive function in AD mice.
- ELISA and Western blot analyzed protein expression (Aβ₁-42, BACE1, p-tau, caspase-3, Bcl-2, GSK-3β, PP2A).
- JC-1 assay evaluated mitochondrial damage in vitro.
Main Results:
- Melatonin significantly improved cognitive function and reduced mitochondrial damage in AD mice.
- Melatonin decreased levels of Aβ₁-42, BACE1, p-tau, GSK-3β, and caspase-3.
- Melatonin increased levels of PP2A and Bcl-2.
Conclusions:
- Melatonin effectively alleviates mitochondrial damage and reduces key proteins associated with AD pathology and apoptosis.
- These actions contribute to the observed improvement in cognitive function in the Aβ₁-42-induced AD mouse model.