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See Inside December 2006

Unlocking Alzheimer's

Understanding the workings of a key protein may presage treatments

With the elderly segment of populations ballooning worldwide, the race to defeat that grim corollary of aging, Alzheimer's disease, is becoming all the more urgent. This year saw several encouraging advances on that front. In what reviewers described as a “technological tour de force,” John R. Cirrito and David M. Holtzman of the Washington University School of Medicine in St. Louis traced production of a destructive Alzheimer's protein, known as amyloid-beta (right), to the junctions between neurons called synapses. They then directly linked high synaptic activity to amyloid-beta increases.

One key to counteracting the devastating effects experienced by patients is detecting the disease early, and another feat by Holtzman, with Randall J. Bateman, also at the Washington University School of Medicine, should make that possible. They have devised a test that measures the manufacture and disposal of amyloid-beta in the brain. Their technique might eventually serve as a basis for detecting the disease early and measuring drug effects on already diagnosed patients.

One of those treatments might someday be based on a synthetic protein fragment that Robert P. Hammer of Louisiana State University has developed to disrupt formation of the plaques believed to provoke massive brain cell death in Alzheimer's patients. The plaques are aggregations of fibers that form when individual amyloid-beta peptides begin sticking together abnormally. Hammer tweaked building blocks of amyloid-beta, synthesizing a nonsticky version of the amino acids that bind the proteins. Adding the engineered fragments to a test tube of normal amyloid-beta blocked the proteins' ability to form fibers, even after four months' exposure. If it does the same in human brains, tens of millions of Alzheimer's sufferers might finally be liberated from a deadly burden of poisonous plaque.

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