Rapamycin reduces neuronal mutant huntingtin aggregation and ameliorates locomotor performance in Drosophila

Huntington’s disease (HD) is a neurodegenerative characterized by movement and cognitive dysfunction. HD caused CAG expansion in exon 1 of the HTT gene that leads to polyglutamine (PQ) repeat huntingtin protein, which aggregates brain periphery. Previously, we used Drosophila models determine Htt-PQ aggregation heart causes shortened lifespan cardiac dysfunction ameliorated promoting chaperonin function or reducing oxidative stress. Here, further study role neuronal mutant how it affects peripheral function. We overexpressed normal ( Htt-PQ25 ) expanded Htt-PQ72 neurons found age-dependent could cause loss synapsin. To if this led dysfunction, performed negative geotaxis assay measure locomotor performance an decrease performance. Next, rapamycin reduced brain. These results demonstrate HD, suggest brain-periphery crosstalk be important pathogenesis show reduces