The preclinical studies mentioned above have suggested that while normal aging may result in decreases in D-serine synthesis and levels, NMDAR activity, the magnitude of LTP and synaptic plasticity (all of which may be reversed by administration of D-serine), pathological aging may involve activation of serine racemase, increased levels of D-serine, NMDAR hyperstimulation and excitotoxicity, resulting in dementia (Table 1). This evidence concerns the gene SRR and dementia.