Chenjian Li

Self-inactivating CRISPR targeting mutant huntingtin in HD mice achieved long-term rescue of neural pathology, motor deficits, weight loss and survival.

This study shows that PINK1 loss causes age-dependent mitochondrial trafficking deficits in dopaminergic neurons via p38 MAPK hyperactivation, leading to impaired mitochondrial motility and increased oxidative stress.

This paper describes the creation of a novel HD mouse model, BAC226Q, which accurately recapitulates age-dependent and progressive HD-like phenotypes.