Decreased Serum Levels of D-Serine in Patients With Schizophrenia

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Abstract
SEVERAL LINES of evidence suggest that a dysfunction in glutamatergic neurotransmission via the N-methyl-D-aspartate (NMDA) subtype of glutamate receptors might be involved in the pathophysiology of schizophrenia.1-6 This hypothesis has evolved from clinical findings that phencyclidine and its congener ketamine, which block the NMDA receptor ion channel, induce a schizophrenia-like psychosis, representing negative and positive symptoms and cognitive dysfunction in healthy humans, and that phencyclidine exacerbates such symptoms in patients with chronic schizophrenia.1,5 Although only L-amino acids generally play a physiologic role in species other than bacteria, the existence of some D-amino acids, such as D-serine in higher species, including humans, has been demonstrated.7-9 It has previously been shown that D-serine is selectively enriched in the forebrain, with immunocytochemical localization in type II astrocytes in gray matter areas also rich in the NMDA receptor,10 suggesting that D-serine may modulate the strychnine-insensitive glycine sites of the NMDA receptor.9 Interestingly, therapeutic trials with D-serine have been shown to significantly improve symptoms (positive, negative, and cognitive) in patients with schizophrenia,11 suggesting that D-serine may play an important role in the pathophysiology of schizophrenia.12 Therefore, it would be of great interest to clarify the potential contribution of endogenous D-serine to the pathophysiology of schizophrenia. Along these lines, the present study was undertaken to examine whether the serum levels of D- and L-serine of patients with schizophrenia are different from those of age- and sex-matched healthy controls.

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