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From the Institute of Child Health (Drs. Hyland, Smith, Clayton, and Leonard), London, and the Clinical Research Center (Mr. Bottiglieri and Dr. Perry), Harrow, United Kingdom; and the Düsseldorf University Childrens Hospital (Dr. Wendel), Düsseldorf, West Germany.
We previously described demyelination in the brain and subacute combined degeneration of the spinal cord in a patient with 5,10-methylenetetrahydrofolate reductase deficiency. To assess the role of methionine, S-adenosylmethionine, folate, and neurotransmitter amine metabolism in the demyelination process, we measured these metabolites in CSF from this patient; the findings are compared with those obtained from three patients in whom neurologic deterioration had been halted by the administration of betaine. Folate concentrations were low, and amine and biopterin metabolism were abnormal in all patients. Methionine and S-adenosylmethionine concentrations were undetectable in the first patient. In those receiving betaine, methionine concentrations were proportional to the dose administered and S-adenosylmethionine concentrations were near normal. The results provide the first evidence for an association between defective S-adenosylmethionine metabolism and demyelination in humans.
Address correspondence and reprint requests to Dr. Hyland, Institute of Child Health, University of London, 30 Guilford Street, London WC1, United Kingdom.
Supported by grants from Action Research for the Crippled Child and the Robert McAlpine Foundation.
Received February 16, 1987. Accepted for publication in final form July 16, 1987.
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