A variety of independent studies have now clearly shown that MLT, in in vitro and in vivo models of neurodegeneration, such as AD and PD, as well as in models of ischemia-reperfusion or in liver damage induced by various agents, decreases the rate of apoptosis, to prevent the formation of the mitochondrial transition pore, to stabilize and maintain the mitochondrial membrane potential and prevent the release of cytochrome c [44,149,150,151]. This evidence concerns the gene CYCS and Alzheimer disease.