Due to technical limitations, our initial understanding of NDD was initially restricted to the pathological manifestations of abnormal protein aggregation, such as Aβ protein in Alzheimer’s disease (AD), huntingtin (HTT) protein in Huntington’s disease, α-synuclein in Parkinson’s disease, and neurofilament in amyotrophic lateral sclerosis. This evidence concerns the gene SNCA and Alzheimer disease.