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Tay-Sachs Disease

These groups have about 100 times the rate of occurrence of other ethnic groups. Approximately one in every 27 Jews in the United States is a carrier of the TSD gene. The carrier rate in the general population is about one in 250. Fewer than 100 children are born with the disease each year in the U.S.
             Tay-Sachs disease is only transmitted through heredity. A Tay-Sachs carrier has one normal gene for hex A and one Tay-Sachs gene. The carrier does not have the illness and leads a normal, healthy and full life. However, when two carriers become parents, there is a one-in-four chance that any child they have will inherit a Tay-Sachs gene from each parent and have the disease. There is a one-in-four chance that the child will inherit the normal gene from each parent and be completely free of the disease and the Tay-Sachs gene. There is a two-in-four chance that the child will inherit one of each kind of gene and be a carrier like the parents and free of disease. A pair of genes on chromosome 15 controls Tay-Sachs disease. These are the genes that code for the enzyme Hex-A. If either or both Hex-A genes are active, the body produces enough of the enzyme to prevent the abnormal build-up of the GM2 ganglioside lipid. .
             The classic infant type of Tay-Sachs disease is the most common. However, there are other rare types of the Hex-A enzyme that sometimes are included under the name of Tay-Sachs disease. These often are referred to as juvenile, chronic and adult-onset forms of Hex-A deficiency. Affected individuals have low levels of the Hex-A enzyme that is missing entirely in the classical infant form. This explains why symptoms begin later in life and are milder than in the classical infant Tay-Sachs disease. Children with juvenile Hex-A deficiency develop symptoms between the ages of 2 and 5 that resemble those of the classical infant form. The process of the disease is slower, but death still occurs by age 15.


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