Notably, as well as responses mediated by CB1, further data showed that the modulation of CB2 signaling, either by using specific CB2 agonists [223,224,225] or by inhibiting 2-AG degrading enzyme MAGL [226], can ameliorate the morphological changes induced by oxidative stress and attenuate cerebral β-amyloid plaque accumulation in a mouse model of Alzheimer’s disease carrying mutated human APPswe and PS1dE9 genes [227,228]. This evidence concerns the gene CNR2 and early-onset autosomal dominant Alzheimer disease.