Activation of microglial cells, as part of a chronic inflammatory response, is a prominent component of AD that drives neurotoxicity through the release of excitotoxins including glutamate, and increased activity of Aβ, which not only promotes glutamate release from microglia, but also stimulates expression of serine racemase and D-serine release from these glial cells (2, 93, 103). This evidence concerns the gene SRR and Alzheimer disease.