By Sudhir Kumar (Eds.)

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Arch. Neurol. (Chicago) 13, 593-614. Austin, J. , Shearer, L. & Briner, O. (1968) Metachromatic leukodystrophy (MLD) VIII. MLD in adults; diagnosis and pathogenesis. Arch. Neurol. (Chicago) 18, 225-240. Balasubramanian, K. A. & Bachhawat, B. K. (1975) Purification properties and glycoprotein nature of arylsulfatase A from sheep brain. Biochim. Biophys. Acta 403, 113-121. Beutler, E. & Kuhl, W. (1972) Biochemical and electrophoretic studies of a-galactoseidase in normal man, in patients with Fabry's disease and in Equidae.

Spranger, J. , Hartman, H. A. Heneberg, B. & Grosse, F. R. (1972) Juvenile G M 1 gangliosidoses: clinical, pathological chemical and enzymatic studies. Clin. Genet. 3, 411434. Okada, S. & O'Brien, J. S. -galactosidase deficiency. Science, 160, 1002-1004. Okada, S. & O'Brien, J. (1969) Tay-Sachs disease: generalized absence of a beta-D-N-acetylhexosaminidase component. Science, 165, 698-700. Opitz, J. (1964) Angiokeratoma corporis diffusum. Arch.

Since both diseases exhibit an autosomal recessive inheritance, it is probable that each is the result of a single gene mutation. The presence of cross-reacting material in both diseases (Srivastava & Beutler, 1974, and Srivastava et al, 1976) METABOLIC DISORDERS IN SPHINGOLIPIDOSES 31 indicates structural gene mutations. Accordingly, this realization implies that, in the case of SandhofTs disease, a single mutation eliminates the activities of two isozymes with relatively unique specificities.

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