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==Clinical applications ==
[[Image:myasthenia.jpg|thumb|left|209px|Patient with myasthenia gravis showing typical symptom of eyelid droop]]
Current research is attempting to learn more about end plate potentials and their effect on muscle activity. Many current diseases involve disrupted end plate potential activity. In Alzheimer patients, [[beta amyloid]] attaches to the acetylcholine receptors and inhibits acetylcholine binding. This causes less signal propagation and small EPPs that do not reach threshold. By analyzing brain processes with acetylcholine, doctors can measure how much beta amyloid is around and use it to judge its effects on Alzheimer's.<ref>Prives J, Professor of Pharmacology, State University of New York at Stony Brook. Interviewed by Pierre Watson. 2008-11-18.</ref>
[[Myasthenia gravis]] is an autoimmune disease, where the body produces antibodies targeted against the acetylcholine receptor on the postsynaptic membrane in the neuromuscular junction. Muscle fatigue and weakness, worsened with use and improved by rest, is the hallmark of the disease. Because of the limited amount of acetylcholine receptors that are available for binding, symptomatic treatment consists of using an acetylcholinesterase inhibitor to reduce the breakdown of acetylcholine in the neuromuscular junction, so that enough acetylcholine will be present for the small number of unblocked receptors
A congenital abnormality caused by a deficiency in end-plate acetylcholine esterase (AChE) might be a pathophysiologic mechanism for myasthenic gravis. In a study on a patient with AChE deficiency, doctors noted that he had developed severe proximal and truncal muscle weakness with jittering in other muscles. It was found that a combination of the jitter and blocking rate of the acetylcholine receptors caused a reduced end-plate potential similar to what is seen in cases of myasthenia gravis.<ref name="Kohara">{{cite journal|doi= 10.1002/mus.10073 |vauthors=Kohara N, Lin TS, Fukudome T, Kimura J, Sakamoto T, etal |year= 2002
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