The observations that NAAG peptidase inhibition and deletion of GCPII are procognitive in control conditions, where the mice have not been cognitively challenged via a drug treatment ([7] and Fig. 1), suggest that the procognitive actions of these peptidase inhibitors in animal models of clinical conditions, such as Alzheimer’s disease (Fig. 2), schizophrenia [8, 11] and ethanol intoxication (Fig. 3), might not be specifically reversing the neurochemical processes that underlie these clinical models but rather be generally procognitive. Here, LAP3 is linked to early-onset autosomal dominant Alzheimer disease.