MicroRNAs: pioneering regulators in Alzheimer's disease pathogenesis, diagnosis, and therapy

被引:8
|
作者
Li, Yao-Bo [1 ]
Fu, Qiang [2 ]
Guo, Mei [3 ]
Du, Yang [2 ]
Chen, Yuewen [4 ,5 ]
Cheng, Yong [1 ,2 ,3 ]
机构
[1] Minzu Univ China, Coll Life & Environm Sci, Ctr Translat Neurosci, Beijing, Peoples R China
[2] Minzu Univ China, Inst Natl Secur, Beijing, Peoples R China
[3] Minzu Univ China, Sch Pharm, Key Lab Ethnomed, Minist Educ, Beijing, Peoples R China
[4] Chinese Acad Sci, Shenzhen Hong Kong Inst Brain Sci Shenzhen Fundame, Brain Cognit & Brain Dis Inst, Shenzhen Inst Adv Technol,Key Lab Brain Connectome, Shenzhen, Peoples R China
[5] HKUST Shenzhen Res Inst, Guangdong Prov Key Lab Brain Sci Dis & Drug Dev, Shenzhen, Peoples R China
来源
TRANSLATIONAL PSYCHIATRY | 2024年 / 14卷 / 01期
基金
中国国家自然科学基金;
关键词
AMYLOID PRECURSOR PROTEIN; PROMOTES TAU PHOSPHORYLATION; IPSC-DERIVED NEURONS; OXIDATIVE STRESS; EARLY-ONSET; UP-REGULATION; MITOCHONDRIAL DYSFUNCTION; SYNAPTIC PLASTICITY; COGNITIVE DECLINE; CELL APOPTOSIS;
D O I
10.1038/s41398-024-03075-8
中图分类号
R749 [精神病学];
学科分类号
100205 ;
摘要
This article delves into Alzheimer's disease (AD), a prevalent neurodegenerative condition primarily affecting the elderly. It is characterized by progressive memory and cognitive impairments, severely disrupting daily life. Recent research highlights the potential involvement of microRNAs in the pathogenesis of AD. MicroRNAs (MiRNAs), short non-coding RNAs comprising 20-24 nucleotides, significantly influence gene regulation by hindering translation or promoting degradation of target genes. This review explores the role of specific miRNAs in AD progression, focusing on their impact on beta-amyloid (A beta) peptide accumulation, intracellular aggregation of hyperphosphorylated tau proteins, mitochondrial dysfunction, neuroinflammation, oxidative stress, and the expression of the APOE4 gene. Our insights contribute to understanding AD's pathology, offering new avenues for identifying diagnostic markers and developing novel therapeutic targets.
引用
收藏
页数:15
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