Importantly, in previous studies, rapamycin treatment decreased plaques and tangles as well as ameliorated cognitive defects in an AD mouse model, prevented dopaminergic neurodegeneration in parkinsonian mice and reduced the levels of mutant ataxin-3 or mutant huntingtin as well as ameliorated their toxicity in vivo, which confirms previous evidence showing that autophagy induction is beneficial in models of neurodegeneration associated with protein aggregates [11, 47, 52, 67, 71]. The gene discussed is ATXN3; the disease is Alzheimer disease.