CNR1 and amyotrophic lateral sclerosis: However, even without considering the still controversial role of CB1R and CB2R and their endogenous agonists (i.e., AEA and 2‐AG) in ALS, it is believed that, in view of the widely documented protective effects of PEA, OEA, EPEA and DHEA via non‐cannabinoid receptors [47], most of the changes observed here represent an attempt to reduce the inflammation and neuronal damage typical of later stages of this disorder.