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Hoppe-Seylers Z. Physiol. Chem. 235, 24-36. Klenk, E. & Schumann, E. (1942) Uber die Ganglioside, des Gehirns bei der infantilen amaurotischen Idiotie von Typus Tay-Sachs. Ber Deutsch. Chem. Ges. 75, 1632-1636. Kolodny, E. , Brady, R. O & Volk, B. W. (1969) Demonstration of an alteration of ganglioside metabolism in Tay-Sachs disease. Biochem. Biophys. Res. Commun. 37, 526-531. Krabbe, K. (1916) A new familial, infantile form of diffuse brain sclerosis. Brain 39, 74-114. Lalley, P. A. & Shows, T.
1967) Purification and separation of four soluble arylsulphatases from ox brain. Enzymologica 32, 169-181. Bowen, D. M. & Radin, N. S. (1968) Purification of cerebroside galactosidase from rat brain. Biochim. Biophys. Acta 152, 587-598. Brady, R. O. (1971) Biochemical approaches to the nosology of nervous system defects, II. In Birth Defect, original article series. Vol. 7, No. 1. (ed. ) The National Foundation March of Dimes, pp. 33-37. Brady, R. , Kanfer, J. & Shapiro, D. (1965) The metabolism of glucocerebrosides.
This type of heterogeneity is observed in other x-linked enzyme deficiencies such as glucose-6-P-dehydrogenease deficiency and also in hypoxanthine-guanine phosphoribosyl transferase deficiency and hemophilia. Variable expression of Fabry's disease in hétérozygote females has been explained by Lyons' hypothesis which predicts that hétérozygotes have two populations of cells, one having the mutant enzyme and the other having the normal enzyme. Occurrence of two such populations in skin fibroblasts has, in fact, been demonstrated in Fabry's disease patients (Romeo & Migeon, 1970).