Amino acid metabolism in endogenous psychoses has been discussed in relation to monoamine synthesis. There are no consistent findings which prove altered monoamine syntheses to be the primary change. Our finding, which suggests decreased amino acid transport across the blood-brain barrier in schizophrenia, does not necessarily mean an insufficient amino acid supply to the brain. Several lines of investigation have shown the possibility of the involvement of glutamatergic dysfunction in the pathogenesis of schizophrenia. Our recent finding of decreased CSF asparagine concentration in schizophrenia and its positive correlation with the response to neuroleptics may support this hypothesis. Recently, free D-serine, an allosteric agonist on NMDA-receptor, has been reported to exist in the rat brain, suggesting that D-serine is an intrinsic ligand. The pathogeneses of endogenous psychoses might be studied in terms of disturbed metabolism of amino acid, as allosteric regulater of neuro-receptor, as well as neurotransmitter and precursor of monoamines.
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