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THOMAS L. PERRY, MD; BLUMA TISCHLER, MD

Am J Dis Child. 1964;107(6):586-589.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

Introduction

In phenylketonuria an enzymatic defect in the liver results in a failure of conversion of phenylalanine to tyrosine. The alternative metabolic pathways followed by the accumulating phenylalanine have been clarified. However, the exact mechanism by which the metabolic error in turn produces mental deficiency in untreated phenylketonurics has not been established. One possible explanation for the mental deficiency was advanced in 1957 by Paré et al¹ who first noted a defect in the 5-hydroxyindole pathway of tryptophan metabolism in phenylketonurics. The presence of serotonin in brain, and the mental abnormalities produced by some serotonin antagonists, have suggested a possible role for this amine in mental function. Paré et al¹ suggested that a failure in serotonin production might play some part in the pathogenesis of the mental defect in phenylketonuria.

Since then it has been demonstrated^2-4 that rats rendered artificially phenylketonuric by the administration of large amounts . . . [Full Text PDF of this Article]

Author Affiliations
VANCOUVER. BC, CANADA; NEW WESTMINISTER. BC. CANADA

Thomas L. Perry, MD, Department of Pharmacology, The University of British Columbia, Vancouver 8, BC, Canada.; From the Department of Pharmacology, University of British Columbia, Vancouver, Canada and The Woodlands School, New Westminster, Canada.

Footnotes
Received for publication Jan 22, 1964.

Supported by grants from the Medical Research Council of Canada, and the Richard W. Lippman Memorial Fund.

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