It has been suggested that with cognitive deficits associated with normal aging and in early AD, there may be decreased expression of serine racemase, decreased levels of D-serine, NMDAR down-regulation and impaired synaptic plasticity, while in advanced AD serine racemase activation and D-serine levels are increased and NMDARs are overstimulated, resulting in excitotoxicity and dementia. This evidence concerns the gene SRR and Cognitive impairment.