MicroRNAs in Alzheimer's disease

被引：208

作者：

Delay, Charlotte ^{[1
,2
]}

Mandemakers, Wim ^{[3
,4
]}

Hebert, Sebastien S. ^{[1
,2
]}

机构：

[1] CHUQ CHUL, Ctr Rech, Quebec City, PQ G1V 4G2, Canada

[2] Univ Laval, Fac Med, Dept Psychiat & Neurosci, Quebec City, PQ G1V 0A6, Canada

[3] Katholieke Univ Leuven, Ctr Human Genet, B-3000 Louvain, Belgium

[4] VIB, Dept Mol & Dev Genet, B-3000 Louvain, Belgium

来源：

NEUROBIOLOGY OF DISEASE | 2012年 / 46卷 / 02期

基金：

加拿大自然科学与工程研究理事会;

关键词：

Alzheimer's disease; MicroRNA; Non-coding RNA; APP; BACE1; Tau; NF-KAPPA-B; PRECURSOR-PROTEIN EXPRESSION; CELL-CYCLE ARREST; AMYLOID-BETA; BRAIN; TAU; INFLAMMATION; DICER; MIRNA; DIFFERENTIATION;

D O I：

10.1016/j.nbd.2012.01.003

中图分类号：

Q189 [神经科学];

学科分类号：

071006 [神经生物学];

摘要：

Alzheimer's disease (AD) is a complex neurodegenerative disorder and is the most common form of dementia in the elderly. Accumulating evidence in AD research suggests that alterations in the microRNA (miRNA) network could contribute to risk for the disease. miRNAs are conserved small non-coding RNAs that control gene expression at the posttranscriptional level and are essential for neuronal function and survival. The results from recent profiling experiments in humans suggest that a number of specific miRNAs are misregulated in disease conditions, several of which have been implicated in the regulation of key genes involved in AD, including APP, BACE1 and MAPT. Moreover, rare disease-specific polymorphisms have been identified in known and putative miRNA target sites located within the 3'untranslated regions (3'UTRs) of APP and BACE1 genes. Here, we review current findings regarding miRNA research in humans and various cellular and animal models to provide a strong basis for future research aimed at understanding the potential contribution of miRNAs to AD pathophysiology. Crown Copyright (C) 2012 Published by Elsevier Inc. All rights reserved.

引用

页码：285 / 290

页数：6

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