This process is mainly caused by the overproduction of Aβ due to mutations in the APP and PS1/2 genes in familial AD, which accounts for 1% of total AD patients, while dysfunction of Aβ clearance is hypothesized to be the main reason for Aβ accumulation in sporadic AD, which accounts for 99% of total AD patients [6]. The gene discussed is APP; the disease is Alzheimer disease.