Saturday, October 23, 2010

Alzheimer's protein may spread through infection

Neurologists have found that the brain plaques associated with Alzheimer's can form when the proteins responsible are injected into the bellies of mice, suggesting that the guilty proteins can get from the body's periphery to wreak havoc in the brain.

A protein called beta-amyloid makes up the brain plaques that accompany the disease. In 2006, Lary Walker at Emory University in Atlanta, Georgia, Mathias Jucker at the University of Tübingen in Germany and colleagues found that they could trigger Alzheimer's-like plaques by injecting samples of plaque-ridden brains into the brains of healthy mice. Now, Jucker and his colleagues at Tübingen have managed to create the same brain plaques by injecting the tissue elsewhere in the bodies of mice.

Mouse models

The group used mice genetically modified to produce large amounts of beta-amyloid, meaning they develop brain plaques similar to those seen in Alzheimer's disease in people. When the mice were around 2 years old, the team removed some of their beta-amyloid-laden brain tissue and injected it into the peritoneum – the lining of the abdomen – of young transgenic mice. Another group of transgenic mice received an injection of healthy brain tissue from normal mice of the same age that had not developed plaques.

Seven months later, before the mice had had a chance to develop plaques of their own accord, the team looked at their brains. The mice injected with healthy brain tissue had normal-looking brains, but those injected with beta-amyloid-heavy tissue had developed full-blown plaques similar to those seen in people with Alzheimer's.

If beta-amyloid in a mouse body's periphery can cause plaques in its brain, could Alzheimer's be transmitted by blood transfusions in humans? There's no evidence to suggest this might be the case, says Jucker. "We don't know if misfolded beta-amyloid can get out of the brain and into the bloodstream, for a start," he says.

Paul Salvaterra, a neurologist at the City of Hope hospital in Duarte, California, points out that Jucker's team only use an indirect measure of Alzheimer's because they focus only on plaques – just one aspect of the disease. "These authors are not studying Alzheimer's disease and certainly not studying infectious Alzheimer's disease," he says. "The type of [disease] they show is only suggestive of some aspects of Alzheimer's disease-related changes in the brain."

The early findings don't yet have implications for the general public, says Jucker, though he cautions that researchers should take care when handling amyloid proteins.

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