Consistent with the role of GCP2 (NAAG hydrolysis), changes in the NAAG levels and/or changes of GCP2 enzymatic activities correlate with pathologic conditions, including Alzheimer’s disease, Huntington’s disease, amyotrophic lateral sclerosis [13,14], epilepsy, schizophrenia [15], and stroke [16]. This evidence concerns the gene FOLH1 and Alzheimer disease.