The pharmacological inhibition of MAGL – thus increasing synaptic availability of 2-AG – with JZL-184 showed the same reversal of acquisition latencies seen in 7-month 3xTg-AD mice as CB1 activation with WIN55212 [132], and improvements in spatial learning and memory with simultaneous repressed β-amyloid accumulation in 5xFAD mice [136]. Here, CNR1 is linked to Alzheimer disease.