Title:MicroRNA-125a-3p Modulate Amyloid β-Protein through the MAPK
Pathway in Alzheimer’s Disease
Volume: 20
Issue: 7
Author(s): Xi-Chen Zhu*, Meng-Zhuo Zhu, Jing Lu, Qing-Yu Yao, Jia-Wei Hu, Wen-Jun Long, Sha-Sha Ruan, Wen-Zhuo Dai and Rong Li*
Affiliation:
- Department of Neurology, the Wuxi No. 2 People's Hospital, Jiangnan University Medical Center, Wuxi, Jiangsu
Province, China
- Brain Institue, Jiangnan University, Wuxi, Jiangsu Province, China
- Department of Neurology, the
Wuxi No. 2 People's Hospital, Affiliated Wuxi Clinical College of Nantong University, Wuxi, Jiangsu Province, China
- Department of Neurology, the Affiliated Wuxi No. 2 People's Hospital of Nanjing Medical University, Wuxi, Jiangsu
Province, China
- Department of Neurology, the
Wuxi No. 2 People's Hospital, Affiliated Wuxi Clinical College of Nantong University, Wuxi, Jiangsu Province, China
- Department of Pharmacy, the Affiliated Wuxi No. 2 People's Hospital, Jiangnan University Medical
Center, Wuxi, Jiangsu Province, China
Keywords:
Alzheimer’s disease, miR-125a-3p, Aβ, fibroblast growth factor receptor 2, MAPK pathway, MicroRNA.
Abstract:
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.
