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TDP-43 DEFICIENCY-INDUCED TRIGLYCERIDE CATABOLISM DISORDER IN ALS: LIPID DROPLETS ACCUMULATION, INSUFFICIENT ENERGY SUPPLY AND NEURONAL DEGENERATION
Tianshuo Zhangand 6 co-authors
The Fifth Affiliated Hospital of Sun Yat-sen University
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS05-09AM-258
Presentation
Date TBA
Board: PS05-09AM-258
Event Information
Poster Board
PS05-09AM-258
Poster
View posterAbstract
The link between TDP-43 gene mutation and abnormal lipid metabolism in amyotrophic lateral sclerosis (ALS) is still unclear. This study initially reveals the manifestations and potential causes of abnormal lipid metabolism in TDP-43 knockout ALS models, as well as its role in pathogenesis of ALS. In this study, neuron-specific TDP-43 knockout mouse model (TDP-43 cKO) with ALS-like phenotype, such as motor deficits, neuronal degeneration and shortened lifespan. Lipid droplet accumulation and elevated triglyceride levels are observed in both TDP-43 cKO mouse and cell models. TDP-43 deficiency downregulates the key enzymes of triglyceride catabolism and impairs lipid transport to mitochondria, thereby reducing ATP supply. However, chlorogenic acid may improve the ALS-like phenotype of TDP-43 cKO mice by promoting triglyceride catabolism and energy production. Triglyceride heptanoate as an easily absorbable lipid supplement, enhances the vitality of ALS cells. Our study confirms TDP-43 deficiency-induced triglyceride catabolism disorder exacerbates ALS progression, and enhancing its metabolism to increase energy supply may represent a potential therapeutic strategy.
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