FOLH1 and brain injury: Inhibition of this proteolytic activity with selective GCPII inhibitors has been shown to be neuroprotective in experiments with mouse models 12; NAAG activation of metabotropic glutamate type 3 receptors exerts neuroprotective effects toward glutamate‐mediated excitotoxicity caused by elevated levels of glutamate released during stroke, traumatic brain injury, and other pathological conditions 13, 14, 15.