It has been shown that MAGL inhibitors (which increase 2-AG levels) reduce the proinflammatory response of microglia and astrocytes, the expression and activity of β-secretase-1 (BACE1), and the Aβ burden in the hippocampus and the temporal and parietal cortices, as well as improve cognitive impairments, in animal models of AD [139,140]. This evidence concerns the gene BACE1 and Alzheimer disease.