Scott P. Allen

This study identifies a common mitochondrial dysfunction phenotype in Leigh syndrome and Huntington's disease patient fibroblasts and finds that the AMPK activator A769662 rescues this phenotype in both conditions.

This study shows that C9orf72-ALS mutation impairs mitophagy in iNeurons by reducing autophagosome production and ULK1 recruitment to mitochondria.

This study shows EPAS1 reduces atherosclerosis at disturbed flow sites by promoting endothelial fatty acid uptake and metabolism, which is suppressed in obesity through triglyceride-PHD3 pathway.

This study shows that activating the Keap1/Nrf2 pathway reduces mitochondrial dysfunction and motor deficits in C9orf72 ALS/FTD models and patient-derived neurons.