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There appear to be several causes of ALS. In 1991 a research team led by Teepu Siddique and Robert H. Brown, Jr. located the gene for familial ALS on chromosome 21. A later discovery pinpointed a mutation in the gene that codes for an enzyme, superoxide dismutase (SOD), as responsible for a percentage of familial cases. These defects do not appear to be present in the more common nonfamilial, or "sporadic," form of the disease. In addition to genetic factors, scientists have studied the buildup of the chemical glutamate that occurs in ALS patients. Glutamate normally acts as a neurotransmitter in the brain, with excess amounts being absorbed by the cells. In ALS patients the reabsorption process fails, and the buildup of glutamate selectively destroys motor neurons. Other possible causes of ALS include defects in the gene that makes the neurofilament proteins that support nerve cell axons, and antibodies that interfere with calcium channels in the cells and cause a toxic buildup of calcium in the neurons.
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