Session Details
[2MS-07]【J】Rethinking FTLD-TDP from novel action of causal proteins
Thu. Nov 28, 2024 3:10 PM - 4:30 PM JST
Thu. Nov 28, 2024 6:10 AM - 7:30 AM UTC
Thu. Nov 28, 2024 6:10 AM - 7:30 AM UTC
Room 7(Fukuoka International Congress Center, 4F 413)
Organizer: Yoshinori Tanaka (Okayama University of Science), Kei Hashimoto (Ochanomizu University)
Frontotemporal lobar degeneration (FTLD) is a type of dementia characteristic of atrophy in the frontal and temporal lobe. FTLD-TDP, featured by a nuclear protein TDP-43 accumulation in the cytoplasm, dominates about a half of FTLD patients. However, it has not been developed to cure FTLD-TDP because of the unknown mechanism. Here we introduce TDP-43 pathology recently reported and novel action of causal proteins of FTLD-TDP, and discuss the mechanism of FTLD-TDP.
[2MS-07-01]Transition from normal to abnormal TDP-43 is caused by failure of autolysosome formation
○Yoshinori Tanaka1 (1. Biochem., Vet. Med., Okayama Univ. of Sci.)
[2MS-07-02]Towards pathological understanding of neurodegenerative diseases by dipeptide repeats derived from aberrant expansion of C9orf72 with a focus on FG motifs
○Yoichi Shinkai1 (1. AIST)
[2MS-07-03]Endogenous retroviral regulation by stress-dependent progranulin expression
○Taku Nedachi1 (1. Toyo Univ.)
[2MS-07-04]Blockade of endo-lysosomal pathway promotes progranulin-deficient microglial toxicity via proinflammatory lipids
○Kei Hashimoto1 (1. Ochanomizu Univ.)