Accordingly, it has been reported similarities to the pathophysiology of aging in the human brain and the early cognitive decline [34] together with other distinctive hallmarks of AD such as Aβ overexpression, upregulation of Presenilin-2 and high levels of p-Tau in the hippocampus, but lower expression of Apolipoprotein-E as compared to their respective control mice [35]. The gene discussed is APOE; the disease is Alzheimer disease.