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The Role of TDP-43 in Alzheimer's Disease

期刊

MOLECULAR NEUROBIOLOGY
卷 53, 期 5, 页码 3349-3359

出版社

HUMANA PRESS INC
DOI: 10.1007/s12035-015-9264-5

关键词

TDP-43; A beta; Tau; Alzheimer's disease; Pathogenesis; Therapy

资金

  1. National Natural Science Foundation of China [81471309, 81371406, 81171209]
  2. Shandong Provincial Outstanding Medical Academic Professional Program
  3. Qingdao Key Health Discipline Development Fund
  4. Qingdao Outstanding Health Professional Development Fund
  5. Shandong Provincial Collaborative Innovation Center for Neurodegenerative Disorders

向作者/读者索取更多资源

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.

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