Arylsulfatase A (ASA) defect and psychiatric illness
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The detection of homozygous (disease state) and heterozygous (carrier) forms of metachromatic leukodystrophy (MLD) and their prevalence among psychiatric individuals are reviewed. Levels of Arylsulfatase A (ASA) activity in peripheral leukocytes, mixed white cell populations, and lymphocytes are compared in normal and psychiatric patients. The prevalence of low levels of enzyme activity in psychiatric patients, and the implications of such levels with regard to the metabolic disease states and associated psychiatric illnesses are discussed. In addition, the use and reliability of leukocyte enzyme assay systems as a criteria for determining and distinguishing between the homozygous and heterozygous conditions are evaluated.
Index EntriesPsychiatric Illness arylsulfatase A defect meta-chromatic leukodystrophy heterozygosity
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- Kolodny E. J. and Moser H. W. (1983) Sulfatide lipidosis: Metachromatic leukodystrophy.The Metabolic Basis of Inherited Disease (Stanbury J. B., Wyngaarden J. B., Fredrickson D. S., Goldstein J. L., and Brown M. S., eds.), pp. 881–905, McGraw Hill, New York, NY.Google Scholar
- Mahon-Hoft H. STone R. K., Johnson R., and Shah S. (1981) Biochemical abnormalities of metachromatic leukodystrophy in an adult psychiatic population.Am. J. Psychiat. 138, 1372–1374.Google Scholar
- Manowitz P., Kling A., and Kohn H. (1978) Clinical course of adult metachromatic leukodystrophy presenting as schizophrenia.J. Nerv. Ment. Def. Dis. 166, 500–506.Google Scholar