Using a transgenic Alzheimer’s disease (AD) mice model, Um et al. found that exercise inhibited the apoptotic cascades, including Bax, cytochrome c, caspase-9 and caspase-3, increased the expression of heat-shock protein-70 (HSP-70) and glucose-regulated protein-78 (GRP-78), and decreased amyloid beta-42 (Abeta-42) peptides significantly [37]. This evidence concerns the gene CASP3 and Alzheimer disease.