Major NDDs have been linked to the accumulation of abnormal protein aggregation in neurons, glial cells, and the extracellular space, such as β-amyloid peptide (Aβ) plaques and tau-positive neurofibrillary tangles (NFTs) in AD [62]; α-synuclein-positive Lewy bodies in PD [63]; tau [64], TDP-43- [65], and FUS-positive aggregates in frontotemporal dementia [66]; and aggregates of a mutant form of huntingtin (HTT) in HD [67]. This evidence concerns the gene HTT and Alzheimer disease.