What I have learned is that cause of ALS has not been identified. The name Amyotrophic Lateral Sclerosis refers only to the symptoms not to a cause. The more I searched the more I came to realize there is probably more than one cause. I will list several areas being studied. Current research suggests an excess of glutamate in the synaptic cleft triggers a cascade of events that ends in cell death.
Glutamate excess is neurotoxic because it over stimulates specific neuronal metabolic functions.
SOD1 normally breaks down free radicals, but mutant SOD1 is unable to perform this function. Accumulation of free radicals leads to nerve cell damage and cell death. 3.Calcium channel antibodies have been isolated which may lead to prolonged influx of calcium into nerve cells, resulting in nerve cell damage and cell death by activating intracellular enzymes. Antibody-mediated calcium increase may also stimulate the release of glutamate, further increasing intracellular calcium and nerve cell damage 4.Some patients have mutations in the gene for neurofilament protein. Studies in mice with this abnormal gene show growth of tangled neurofilaments that block mitochondria from reaching the nerve cell axon, causing nerve cell death.