{"id":24989,"date":"2024-12-16T09:43:19","date_gmt":"2024-12-16T08:43:19","guid":{"rendered":"https:\/\/idibell.cat\/en\/?post_type=agenda&p=24989"},"modified":"2024-12-16T09:46:46","modified_gmt":"2024-12-16T08:46:46","slug":"idibellseminars-c9orf72-ftd-als-mechanisms-and-therapeutic-approaches","status":"publish","type":"agenda","link":"https:\/\/idibell.cat\/en\/agenda\/idibellseminars-c9orf72-ftd-als-mechanisms-and-therapeutic-approaches\/","title":{"rendered":"#IDIBELLseminars: C9orf72 FTD\/ALS: mechanisms and therapeutic approaches"},"content":{"rendered":"

A GGGGCC repeat expansion in C9orf72 is the most common genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). I will describe recent work using iPSC-neurons, patient tissue and novel mouse and Drosophila models to gain new mechanistic insights into disease pathogenesis and neuroprotective pathways. This will include a new role for lipid alterations in FTD\/ALS and a novel gene therapy approach to combat C9orf72 repeat pathologies.<\/span><\/p>\n

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