Laboratory experiments have also shown that caffeine treatment can improve working memory and decrease brain Aβ loads in mouse models of AD via suppression of both β-secretase (BACE1) and presenilin 1 (PS1)/γ-secretase expression (Arendash et al., 2006, 2009), and improve locomotor function and attenuate dopamine depletion in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) induced toxicity model of PD in mice (Chen et al., 2001; Xu et al., 2010). This evidence concerns the gene BACE1 and Alzheimer disease.