Keeping Amyloid–and Alzheimer's–in Check
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Researchers have identified a protein that reins in the rogue activity of the molecules that make the amyloid-beta protein—which may prevent normal brain function in people with Alzheimer's disease. Their findings reveal a potentially powerful tool for designing novel Alzheimer's treatments.
Amyloid beta-peptides are sticky, neurotoxic protein fragments that accumulate, kill nerve cells, and clump together to form the distinctive amyloid plaques in the brains of people with Alzheimer's disease. They are generated when a larger, normal protein called amyloid precursor protein (APP) is cleaved or split in a series of events. A protein complex called the presenilin complex is responsible for the final cleavage event.
Presenilin complexes are thought to cause an unusual form of protein cleavage in which selected membrane proteins are split in a region that crosses cell membranes. This previously unrecognized form of protein cleavage is essential for several normal signaling processes.

Further investigation of the regulatory proteins controlling presenilin complexes may reveal other potential targets for drugs to treat Alzheimer's disease, which affects as many as 4.5 million Americans and nearly half a million Canadians. Up to now, attempts to develop medicines to inhibit amyloid-beta production have been hindered, the researcher said, because they frequently inhibit the normal and essential signaling functions too.

Alzheimer's theory set for drug testSeattle Post Intelligencer - USA... Now, researchers are hunting new ones that target the disease's hallmark, a sticky gunk called beta-amyloid that clogs up, and probably kills, neurons. ...