Enhanced insulin signalling ameliorates C9orf72 toxicity in Drosophila
16 April 2021
A hexanucleotide repeat expansion (HRE) in the c9orf72 is the most common genetic cause of ALS and FTD, complex neurodegenerative diseases with no efficient treatment available. Activation of insulin signalling could be a future therapeutic approach.
Understanding the key downstream molecular pathways dysregulated in c9ALS/FTD is crucial to provide promising molecular targets for future therapeutic intervention for ALS and FTD. Using an HRE neurodegeneration fly model we found that insulin signalling is reduced and that activation of insulin signalling could be a future therapeutic approach.