In addition, our laboratory previously reported that reduced levels of VDAC1 may lead to decreased interaction between VDAC1 and APP, Aβ, and phosphorylated Tau and may allow mitochondrial pore opening and pore closure, ultimately leading to normal mitochondrial function and synaptic ATP and boosting synaptic and cognitive functions in AD (Manczak & Reddy, 2012). Here, APP is linked to Alzheimer disease.