Patients with ALS and reactive gliosis were shown to have an elevated level of CB2 in the spinal cord- and cortical motor neurons, as well as astrocytes but no changes, were observed in CB1, MAGL, or FAAH (Espejo-Porras et al., 2018a).
In the TDP-43 (A315T) mouse model of ALS, reactive gliosis can be reduced by THC-like substances. Also, motor performance can be ameliorated by THC-like substances via CB2 (Espejo-Porras et al., 2018b).
In the hSOD (G93A) mouse model of ALS, THC can help in preventing neuronal excitotoxicity, ameliorating motor performance, and increasing survival by 5% (Raman et al., 2004; Urbi et al., 2018).
In the hSOD(G93A) mouse model of ALS, it was shown that elevation of 2AG by MAGL inhibition can play a role in shielding against inflammation and neurodegeneration (Pasquarelli et al., 2017).
In the hSOD(G93A) mouse model of ALS, a synthetic cannabigerol derivative exhibited protective effects against reactive gliosis, preserved motor neurons, and attenuated weight loss via pparγ (Rodríguez-Cueto et al., 2018).