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The Role of TDP‐43 in the Pathogenesis of Frontotemporal lobar degeneration
Author(s) -
Tsai KuenJer
Publication year - 2018
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2018.32.1_supplement.805.12
Subject(s) - frontotemporal lobar degeneration , frontotemporal dementia , amyotrophic lateral sclerosis , pathogenesis , biology , ubiquitin , dna damage , programmed cell death , semantic dementia , pathology , dementia , microbiology and biotechnology , gene , dna , medicine , disease , genetics , apoptosis
Frontotemporal lobar degeneration (FTLD) is one of the most common neurodegernation diseases, especially in the dementia. TDP‐43 is a multifunctional DNA/RNA‐binding factor, which has been identified as the major disease protein of frontotemporal lobar degeneration with ubiquitin‐positive inclusions (FTLD‐U) and amyotrophic lateral sclerosis (ALS). TDP‐43 has been known mainly as a nuclear protein, with two RNA‐recognition motifs (RRM), RRM1 and RRM2, and a glycine‐rich region in its C‐terminus. However, the role of TDP‐43 in the pathogenesis of FTLD‐U has remained unknown. Therefore, to know how TDP‐43 pathology results in neuronal death in FTLD‐U may provide a therapeutic strategy to FTLD‐U. In this study, to test whether aberrant cell cycle activity and DNA damage involve in the neuronal death results from TDP pathology, the expression level of cell cycle associated genes and DNA damage marker had been examined. Form the result, cell cycle re‐expression and DNA damage occur in the TDP‐43 Tg mice and human brain tissues. This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .