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