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Reversing early sign of alzheimer's - animal experiment successful,for a while by ferujkll sdff





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Reversing early sign of alzheimer's - animal experiment successful,for a while by
Article Posted: 06/20/2012
Article Views: 83
Articles Written: 2023
Word Count: 588
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Reversing early sign of alzheimer's - animal experiment successful,for a while


 
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A researcher from an investigation led by Case Western ReserveUniversity School of Medicine, has discovered that removing aplaque-forming protein in a mouse model of Alzheimer's disease , can restore one of the earliest known impairments caused by thedisease - loss of sense and smell. A summary of the study ispublished in the Nov. 2 issue of The Journal of Neuroscience . The investigation verifies that the protein (amyloid beta) isresponsible for the loss of sense and smell.



Daniel Wesson, assistant professor of neuroscience at Case WesternReserve and lead investigator, explains: "The evidence indicates we can use the sense of smell to determineif someone may get Alzheimer's disease, and use changes in sense ofsmell to begin treatments, instead of waiting until someone hasissues learning and remembering. We can also use smell to see iftherapies are working." Numerous ailments, exposures and injuries can cause loss of smell.Since the 1970's, loss of smell has been identified as an earlysign of Alzheimer's. The novel investigation demonstrates theregion in the brain and how this happens, and that it can betreated. Wesson, states: "Understanding smell loss, we think, will hold someclues about how to slow down this disease." At present there is no effective treatment or cure for Alzheimer's,marked by deteriorating senses, cognition and coordination,eventually leading to death.



Currently in the U.S., 5.3 millionindividuals suffer from the disease, and according to theAlzheimer's Association, this number is predicted to triple to 16million by 2050. Wesson collaborated with Anne H. Borkowski, an investigator at theNathan S. Kline Institute in Orangeburg, N.Y., Gary E.



Landreth,professor of neuroscience at Case Western Reserve School ofMedicine, and Ralph A. Nixon, Efrat Levy and Donald A. Wilson, ofthe New York University School of Medicine. The researchers discovered that just a minuscule amount of amyloidbeta (too little to be seen on current brain scans) causes mousemodels to lose their sense of smell.



They found that the plaque protein gathered initially in parts ofthe brain linked to smell, long before it started building up inregions connected with cognition and coordination. Early on, the olfactory bulb, where odor information from the noseis processed, became hyperactive. However, over time, the level of the protein increased in theolfactory bulb, making it hypoactive (not active enought). Eventhough the mice spent more time sniffing, they were unable toremember smells and became incapable of telling different odorsapart.



The same pattern is observed in individuals with Alzheimer's, asthey age they become unresponsive to smells. Although researchers observed losses in the olfactory system, therest of the mouse model brain, including the hippocampus, which isthe center for memory, continued to act normally in the early stageof Alzheimer's. Wesson explains: "This shows the unique vulnerability of the olfactory system to thepathogenesis of Alzheimer's disease." The researchers then set out to reverse the effects. They gave themice a synthetic liver x-receptor agonist, a medication thatremoves amyloid beta from the brain. After two weeks of treatmenton the drug, the mice were able to process smells normally.However, one week after withdrawal of the drug, impairmentsreturned.



Wesson and his team are currently following-up on these findings tofind out how amyloid spreads throughout the brain, in order tolearn techniques to slow progression of the disease. Written by Grace Rattue Copyright: Medical News Today Not to be reproduced without permission of Medical News Today Additional References Citations.

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