| Literature DB >> 26081142 |
Xiao-Long Chang1, Meng-Shan Tan2, Lan Tan3,4, Jin-Tai Yu5,6.
Abstract
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 β-amyloid (Aβ)-dependent and Aβ-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.Entities:
Keywords: Alzheimer’s disease; Aβ; Pathogenesis; TDP-43; Tau; Therapy
Mesh:
Substances:
Year: 2015 PMID: 26081142 DOI: 10.1007/s12035-015-9264-5
Source DB: PubMed Journal: Mol Neurobiol ISSN: 0893-7648 Impact factor: 5.590