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
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.)
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[2MS-07-03]Endogenous retroviral regulation by stress-dependent progranulin expression

○Taku Nedachi1 (1. Toyo Univ.)
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[2MS-07-04]Blockade of endo-lysosomal pathway promotes progranulin-deficient microglial toxicity via proinflammatory lipids

○Kei Hashimoto1 (1. Ochanomizu Univ.)
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