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Kynurenine metabolites of tryptophan

Implications for neurologic diseases

Department of Neurology (A. Freese and K. J. Swartz, and Drs. During and Martin), Massachusetts General Hospital and Harvard Medical School, Boston, MA; the Division of Health Sciences and Technology (A. Freese), Massachusetts Institute of Technology, Cambridge, MA; Program in Neuroscience (K.J. Swartz), Harvard Medical School, Boston, MA; and the Departments of Pharmacology and Psychiatry (Dr. During), Yale University School of Medicine, New Haven, CT. Dr. Martin's current address is Office of the Dean, University of California, San Francisco, CA.

Over the past 2 decades, a number of studies have demonstrated that amino acids act as precursors for the biosynthesis of a variety of neuroactive compounds, including catecholamines and indoleamines. For example, the aromatic amino acid l-tryptophan is a precursor for serotonin biosynthesis. Based on this observed precursor relationship, dietary tryptophan supplementation is used to treat a number of neurologic disorders attributed to alterations in serotoninergic neurotransmission. Recent studies have revealed that, in addition to serotonin, a number of neuroactive compounds, the kynurenines, are metabolities of tryptophan. Of these, perhaps the most important is quinolinic acid, a neurotoxin that acts at the N-methyl-d-aspartate (NMDA) receptor and whose precursor responsiveness to tryptophan far exceeds that of serotonin. In the central nervous system, kynurenines, and in particular quinolinic acid, may modulate excitatory amino acid transmission, and may act as neurotoxic agents implicated in the pathogenesis of several neurologic diseases.

Address correspondence and reprint requests to Andrew Freese, Neurology Research, Edwards 4, Massachusetts General Hospital, Fruit Street, Boston, MA 02114

Received April 28, 1989. Accepted for publication in final form September 13, 1989.

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