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MicroRNA-125a-3p Modulate Amyloid β-Protein through the MAPK Pathway in Alzheimer's Disease
Xi-Chen Zhu1,2,3,4, Meng-Zhuo Zhu3, Jing Lu4
1Department of Neurology, the Wuxi No. 2 People's Hospital, Jiangnan University Medical Center, Wuxi, Jiangsu Province, China.
Background:
MicroRNA (miR)-125a-3p is reported to play an important role in some central nervous system diseases, such as Alzheimer's disease (AD). However, a study has not been conducted on the mechanism of miR-125a-3p in the pathological process of AD.
Methods:
First, we assessed the expression of miR-125a-3p in AD cohort. Subsequently, we altered the expressions of miR-125a-3p to assess its role in cell viability, cell apoptosis, amyloid-β (Aβ) metabolism, and synaptic activity. Finally, we identified its potential mechanism underlying AD pathology.
Results:
This study unveiled the potential function of miR-125a-3p through modulating amyloid precursor protein processing. Additionally, miR-125a-3p influenced cell survival and activated synaptic expression through the modulation of Aβ metabolism in the mitogen-activated protein kinase (MAPK) pathway via fibroblast growth factor receptor 2.
Conclusion:
Our study indicates that targeting miR-125a-3p may be an applicable therapy for AD in the future. However, more in vitro and in vivo studies with more samples are needed to confirm these results.
Insights
MicroRNA 125a-3p influences Alzheimer's disease (AD) pathology by modulating amyloid precursor protein processing and Aβ metabolism. Targeting this microRNA may offer a future therapeutic strategy for AD.
Area of Science:
- Neuroscience
- Molecular Biology
- Genetics
Background:
- MicroRNA (miR)-125a-3p is implicated in central nervous system diseases, including Alzheimer's disease (AD).
- The precise mechanism of miR-125a-3p in AD pathogenesis remains unelucidated.
Purpose of the Study:
- To investigate the role and mechanism of miR-125a-3p in the pathological processes of Alzheimer's disease.
- To assess the impact of miR-125a-3p on cellular functions relevant to AD.
Main Methods:
- Assessed miR-125a-3p expression in an Alzheimer's disease cohort.
- Manipulated miR-125a-3p levels to evaluate effects on cell viability, apoptosis, amyloid-β (Aβ) metabolism, and synaptic activity.
- Identified the underlying molecular mechanism.
Main Results:
- miR-125a-3p modulates amyloid precursor protein processing and Aβ metabolism.
- miR-125a-3p influences cell survival and synaptic activity via the MAPK pathway, involving fibroblast growth factor receptor 2.
- Aβ metabolism modulation by miR-125a-3p impacts synaptic expression.
Conclusions:
- miR-125a-3p plays a significant role in AD pathology.
- Targeting miR-125a-3p presents a potential therapeutic avenue for Alzheimer's disease.
- Further in vitro and in vivo studies are warranted to validate these findings.
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