These changes included both hyper- and hypoactivity of CB1R signaling, increased levels of 2-AG and AEA, and altered expression of CB1R and CB2R in the basal ganglia of people with PD and transgenic mice including 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-lesioned mouse models and lipopolysaccharide (LPS) rat models [85,86,87]. This evidence concerns the gene CNR1 and Parkinson disease.