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New avenues in search for Alzheimer’s cure

Date:
July 14, 2014
Source:
American Technion Society
Summary:
Researchers shed new light on key mechanism in accumulation of protein plaques in Alzheimer’s disease patients, which could open new avenues for developing a cure for Alzheimer's disease, which affects 5.2 million in the U.S. alone. The researchers' breakthrough findings are centered on UBB +1, a mutation prevalent in Alzheimer's disease patients. The mutation impairs a protein called ubiquitin that marks other proteins to be dismantled at the proteasome.
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Alzheimer's disease affects approximately 5.2 million people in the United States alone, and it is the nation's sixth leading cause of death. A cure for this insidious killer has so far proven elusive, but that could soon change as a result of a breakthrough at the Technion-Israel Institute of Technology that sheds light on a key mechanism in the accumulation of protein plaques in the tissue of Alzheimer's disease patients.

The findings were published online last week in Nature Chemical Biology.

"Proteins that constitute major building blocks of our body cells continuously pass through quality control," explains team leader Prof. Michael Glickman, of the Faculty of Biology. "Defective proteins are sent to the proteasome, a molecular machine (found in all of our cells) that eliminates defective proteins by recycling them back to their building blocks. But a small number of them slip through this process. Proteins that evade the proteasome accumulate, and may be harmful when they reach a critical mass, which is often the case at an advanced age."

The researchers' breakthrough findings are centered on UBB +1, a mutation prevalent in Alzheimer's disease patients. The mutation impairs a protein called ubiquitin that marks other proteins to be dismantled at the proteasome.

Previously, the prevailing view among scientists was that UBB +1 impairs the functioning of the proteasome itself. But in her doctoral dissertation under the guidance of Prof. Glickman, Dr. Daria Krutauz found that in the presence of UBB+1, damaged proteins are apprehended on their way to the proteasome, and accumulate without reaching their final recycling destination. As a result, they have more opportunity to form the deadly plaque associated with Alzheimer's disease.

"Because our findings run contrary to what was previously believed, this discovery opens new venues for intervention in the hope of developing a cure for Alzheimer's disease," says Prof. Glickman.


Story Source:

The above post is reprinted from materials provided by American Technion Society. The original item was written by Kevin Hattori. Note: Materials may be edited for content and length.


Journal Reference:

  1. Daria Krutauz, Noa Reis, Mark A Nakasone, Peter Siman, Daoning Zhang, Donald S Kirkpatrick, Steven P Gygi, Ashraf Brik, David Fushman, Michael H Glickman. Extended ubiquitin species are protein-based DUB inhibitors. Nature Chemical Biology, 2014; DOI: 10.1038/nchembio.1574

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American Technion Society. "New avenues in search for Alzheimer’s cure." ScienceDaily. ScienceDaily, 14 July 2014. <www.sciencedaily.com/releases/2014/07/140714122610.htm>.
American Technion Society. (2014, July 14). New avenues in search for Alzheimer’s cure. ScienceDaily. Retrieved August 4, 2015 from www.sciencedaily.com/releases/2014/07/140714122610.htm
American Technion Society. "New avenues in search for Alzheimer’s cure." ScienceDaily. www.sciencedaily.com/releases/2014/07/140714122610.htm (accessed August 4, 2015).

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