Amyotrophic lateral sclerosis: hypothetical pathogenesis.
A hypothetical pathogenesis for a typical case of amyotrophic lateral sclerosis (ALS) follows from opinions of Rowland and results of neuroscientists at Baylor. ALS might typically result from an autoimmune disorder that causes IgG to enhance release of acetylcholine (ACh) from axon terminals. Motor neuron overactivity associated with fasciculation might result from enhanced release of ACh which is taken up by nicotinic ACh receptors. Increased levels of intracellular calcium ions might result from motor neuron overactivity associated with fasciculation. Neuronal cell degeneration and death might result from increased levels of intracellular calcium ions.
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D000109:Acetylcholine / Q000378:metabolism*; D000690:Amyotrophic Lateral Sclerosis / Q000209:etiology* / Q000276:immunology; D000818:Animals; D001327:Autoimmune Diseases / Q000150:complications* / Q000503:physiopathology; D002118:Calcium / Q000378:metabolism; D005207:Fasciculation / Q000503:physiopathology; D006801:Humans; D007074:Immunoglobulin G / Q000502:physiology*; D007473:Ion Channels / Q000378:metabolism; D008954:Models, Biological; D009046:Motor Neurons / Q000502:physiology*; D009410:Nerve Degeneration; D011188:Potassium / Q000378:metabolism; D011978:Receptors, Nicotinic / Q000502:physiology; D009435:Synaptic Transmission
D007074:Immunoglobulin G; D007473:Ion Channels; D011978:Receptors, Nicotinic; D000109:Acetylcholine; D011188:Potassium; D002118:Calcium