In animal AD models, they showed anti-amyloidogenic effects, reduced cerebral plaques and soluble and fibrillar Aβ-species, suppressed cerebral inflammation and alterations in tau protein and inhibited Aβ-induced apoptosis through various mechanisms including elevating sAPPa levels, decreasing Bax/Bcl-2 ratio and cleaved caspase-3 level, decreasing in Aβ40 and Aβ42, reducing NO release from microglia, activation of SIRT1 and AMPK pathways, etc. (33, 37, 60). This evidence concerns the gene BCL2 and Alzheimer disease.