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Found: A New Piece in the Alzheimer's Puzzle
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Found: A New Piece in the Alzheimer's Puzzle


A team of researchers from three different countries have reported that a tiny portion of a protein implicated in Alzheimer’s disease may be so crucial that it could unlock the door to effective new treatments. Alzheimer’s affects approximately 5% of adults between the ages of 65 and 74, and risk for the disease goes up steadily with age.

These plaques are responsible for the breakdown in communication between brain cells that leads to the cognitive decline seen in affected individuals.

The researchers, reporting the September issue of The FASEB Journal studied a fragment of the RanBP9 protein called N60, which is thought to facilitate the formation of beta amyloid plaques in the brains of Alzheimer’s patients. These plaques are responsible for the breakdown in communication between brain cells that leads to the cognitive decline seen in affected individuals. Researchers have long been looking for a way to slow or reverse the development of these plaques in hopes of finding an effective treatment for the disease.

The team, led by David Kang, at the University of California, San Diego, compared samples of brain cells of Alzheimer’s patients to those of healthy patients, and measured the degree to which N60 was present in both groups of cells. They found that the protein fragment was considerably increased in the Alzheimer’s brains. In another test, the researchers expressed full−length RanBP9 DNA, RanBP9−N60 DNA, and control DNA in brain cells that were unaffected by Alzheimer’s. What they found was that in the full−length RanBP9 cultures, there were significantly more plaques – three times more – than in controls. But even more striking was the finding that in the RanBP9−N60 cultures plaque levels were present in five times the numbers seen in control samples.

Kang says that the findings “[suggest] that targeting RanBP9 expression and/or N60 fragment generation may lead to novel strategies to combat this devastating disease." The more researchers are able to home in on the biology behind Alzheimer’s, the more likely they will be to devise a specific treatment to target these mechanisms. Editor−in−Chief of The FASEB Journal Gerald Weissmann says that studies like this really do offer hope: “Alzheimer's might seem hopeless to some, but this research shows that we're closer than ever to unraveling both the protein tangles and mysteries surrounding this devastating disease."

October 1, 2009


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