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Cause Behind Alzheimer's Plaques Identified
In the new study, led by Gen He, a research associate in Greengard's lab, the researchers showed that GSAP stimulates production of beta-amyloid in cell lines, and that reducing GSAP reduces beta-amyloid. The researchers also looked at GSAP's action in a mouse model of Alzheimer's disease. They knocked down the gene that codes for GSAP using RNA interference, and found that levels of beta-amyloid as well as plaque development decreased. Biochemical studies showed that Gleevec reduces beta-amyloid production by binding to GSAP and preventing its activation of gamma-secretase.
Unfortunately, the Gleevec molecule does not cross the blood-brain barrier, the gatekeeper that prevents some substances in the blood from entering the brain. Greengard, however, believes that it will be possible to design drugs that target GSAP but do not have this limitation.
"Anti-amyloid therapeutic drugs represent a valid approach to treating Alzheimer's disease, but their inability to accumulate in the brain has limited their usefulness," says Greengard, who is head of the Laboratory of Molecular and Cellular Neuroscience. "The development of compounds that work like Gleevec, but have the ability to pass the blood-brain barrier and target GSAP could revolutionize the treatment of this disease."
Source-Eurekalert
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