Genes associated with familial neurodegenerative diseases in humans and proteins associated with disease pathophysiology, such as Aβ, mutated tau (Alzheimer’s disease), α-synuclein, mutated Pink, Parkin and Dj-1 (Parkinson’s disease), mutated Huntingtin and a polyglutamine tract (Huntington’s disease and ataxia) caused neuropathologies in flies that are very similar to what was observed in human patients [52,53,54]. Here, HTT is linked to juvenile Huntington disease.