Based on all these observations, lowering the levels of VDAC1, Aβ, and P-tau could reduce the interactions between VDAC1 and Aβ and between VDAC1 and phosphorylated tau in AD neurons, resulting in the maintenance of normal opening and closing of mitochondrial pores and then in the normal functioning of mitochondria supplying ATP to nerve endings (as is the case with healthy neurons). This evidence concerns the gene MAPT and Alzheimer disease.