The Role of TDP-43 in Alzheimer's Disease

被引：72

作者：

Chang, Xiao-Long ^{[1
]}

Tan, Meng-Shan ^{[2
]}

Tan, Lan ^{[1
,2
]}

Yu, Jin-Tai ^{[2
,3
]}

机构：

[1] Dalian Med Univ, Qingdao Municipal Hosp, Dept Neurol, Qingdao, Peoples R China

[2] Qingdao Univ, Sch Med, Qingdao Municipal Hosp, Dept Neurol, Qingdao 266071, Peoples R China

[3] Univ Calif San Francisco, Dept Neurol, Memory & Aging Ctr, San Francisco, CA USA

来源：

MOLECULAR NEUROBIOLOGY | 2016年 / 53卷 / 05期

基金：

中国国家自然科学基金;

关键词：

TDP-43; A beta; Tau; Alzheimer's disease; Pathogenesis; Therapy; AMYOTROPHIC-LATERAL-SCLEROSIS; TAR-DNA-BINDING; FRONTOTEMPORAL LOBAR DEGENERATION; MOTOR-NEURON DISEASE; MOUSE MODEL; PROTEIN; 43; MITOCHONDRIAL DYSFUNCTION; TRANSGENIC MICE; NEURODEGENERATIVE DISEASES; PARKINSONS-DISEASE;

D O I：

10.1007/s12035-015-9264-5

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

The transactive response DNA binding protein (TDP-43) has long been characterized as a main hallmark of amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration with ubiquitin-positive inclusions (FTLD-U, also known as FTLD-TDP). Several studies have indicated TDP-43 deposits in Alzheimer's disease (AD) brains and have robust connection with AD clinical phenotype. FTLD-U, which was symptomatically connected with AD, may be predictable for the comprehension of the role TDP-43 in AD. TDP-43 may contribute to AD through both beta-amyloid (A beta)-dependent and A beta-independent pathways. In this article, we summarize the latest studies concerning the role of TDP-43 in AD and explore TDP-43 modulation as a potential therapeutic strategy for AD. However, to date, little of pieces of the research on TDP-43 have been performed to investigate the role in AD; more investigations need to be confirmed in the future.

引用

页码：3349 / 3359

页数：11

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