Notably, multiple effects on mitochondrial function and on the apoptotic pathway that seems to be crucial for its beneficial effects in AD were reported: stabilization of mitochondrial membrane potential, improvement of energy metabolism, up-regulation of anti-apoptotic Bcl-2 protein and down-regulation of pro-apoptotic Bax protein, inhibition of cytochrome c release, reduction of caspase 9 and caspase 3 activity after oxidative stress and reduction of apoptotic cell death [8]–[14]. The gene discussed is CASP3; the disease is Alzheimer disease.