AD, which is typified by neurofibrillary tangles (NFTs) and the aggregation of senile plaques that are formed by the amalgamation of amyloid-β protein, a truncated product of APP (Amyloid precursor protein) cleaved by the enzyme β-secretase (BACE1), is the foremost contributor to NDDs (Xie et al. 2014). The gene discussed is APP; the disease is Senile plaques.