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What might be done with the cases that are not diagnosed prenatally? The main concern at present is to try to replace the missing enzyme. This is quite a complicated process. We have purified hexosamini­ dase A to homogeneity from human urine and expect to undertake enzyme infusion studies, with appropriate precautions, into Tay-Sachs patients. We do not know how effective such replacement therapy will be b e ­ cause of the uncertainty that the enzyme can pass across the blood brain barrier. If it does not reach the brain, other procedures will have to be consid­ ered (cf.

B R A D Y 0 Fig. 32. 2 4 6 8 10 12 DISTANCE (cm) 14 16 Ganglioside labelling pattern of hepatocytes and Morris hepatoma Η 4123 using N-acetyl% - D - m a n n o s a m i n e as precursor in tissue cullure. Acknowledgments Figure 3 is reproduced from Lipids and Lipido­ ses , G. , 1967, page 318. B. B. S. Fredrickson, editors, Second Edition, McGraw-Hill Book Company, New York, 1966, page 567. Figure 13 from the same source, page 593 and Figure 1 8 , page 621. D. Terry and M. Weiss: Studies in Tay-Sachs Disease.

What practical use can we make of this informa­ tion? In all of these diseases there are two very important clinical aspects which can now be elucida­ ted. The first is the detection of carriers of these diseases. Heterozygote detection is somewhat tenuous because there is only a partial deficiency of the en­ zyme involved, and probably only a few types of cells, such as leukocytes and cultured fibroblasts are suit­ able for such tests. We have frequently used soni­ cated fresh white blood cell preparations (Table 12 and 13) and extracts of cultured skin fibroblasts for the identification of carriers ( 4 ) .

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