updated 9/21/2006 6:09:01 PM ET 2006-09-21T22:09:01

Scientists injected a sticky goo from Alzheimer’s victims into the brains of mice and watched it take over, provocative research that promises to help shed new light on the earliest stages of the memory-robbing disease.

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No one knows if this sticky protein, called beta-amyloid, actually causes Alzheimer’s, but it is the chief suspect, and the study reported Thursday adds to the evidence.

The German-led study found a tiny clump of bad beta-amyloid triggers a buildup that results in Alzheimer’s hallmark brain-crusting plaques — by physically pushing nearby healthy proteins into rotten shapes.

“It’s a very exciting paper,” said Dr. Sam Gandy, a neuroscientist and amyloid expert at Philadelphia’s Thomas Jefferson University who assessed the study on behalf of the Alzheimer’s Association.

“This may give us a novel way to try and understand the way amyloid changes its shape to become toxic, become poisonous,” he explained.

Moreover, there appear to be different strains of abnormal amyloid, lead researcher Mathias Jucker, a neurology professor at Germany’s University of Tubingen, reported in the journal Science. If scientists can determine which version drives plaque buildup, it may point to ways to attack Alzheimer’s before it gains too big a hold on the brain, he said.

“Identification of this misfolded, initiating a-beta — that will be the big thing,” Jucker said.

About 4.5 million Americans have Alzheimer’s, a toll expected to more than triple by 2050 as the population grays. The creeping brain disease gradually robs sufferers of their memories and ability to care for themselves, eventually killing them. There is no known cure; today’s drugs only temporarily alleviate symptoms.

All brains contain beta-amyloid, although healthy cells somehow get rid of excess amounts. But in Alzheimer’s patients’ brains, abnormal beta-amyloid builds up into distinctive clumps, or plaques.

What makes good beta-amyloid turn bad is a mystery.

Domino effect
But the new study suggests that once that first little clump forms, it acts as a seed that corrupts nearby healthy amyloid, said co-author Lary Walker of Emory University’s Yerkes National Primate Research Center in Atlanta.

It’s similar to how one crystal can spark others to form, a domino effect very similar to that seen in mad cow disease and other neurodegenerative diseases that are caused by abnormally shaped proteins called prions.

Don’t be alarmed: No one is suggesting Alzheimer’s is infectious like prion diseases are, both Walker and Gandy stressed. Scientists were able to trigger Alzheimer’s-like plaques in the mouse brains only because they used mice genetically engineered to be particularly vulnerable to human amyloid — they were going to get sick anyway, but the “seeds” hastened the process.

First, Jucker triggered plaques by injecting mice with brain tissue from a few Alzheimer’s patients. Then, for a closer look at how the amyloid “seeds” spread, he repeated the experiment by injecting amyloid from mice into other mice — and that’s where he spotted varying strains of abnormal amyloid that look and act differently from one another.

Maybe there are a lot of ways amyloid can become misshapen but only a few are poisonous to the brain, suggested Gandy, who said the study should stimulate development of technology to better examine the protein and figure that out.

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