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Blood sugar loss may trigger Alzheimer's: study
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A slow, chronic reduction of blood sugar to the brain could trigger some forms of Alzheimer's disease, U.S. researchers said on Wednesday.

The study of human and mice brains suggests a reduction of blood flow deprives energy to the brain, setting off a process that ultimately produces the sticky clumps of protein researchers believe is a cause of the disease, they said.

The finding could lead to strategies such as exercise, reducing cholesterol and managing blood pressure to keep Alzheimer's at bay, Robert Vassar and colleagues at Northwestern University's Feinberg School of Medicine in Chicago reported.

"This finding is significant because it suggests that improving blood flow to the brain might be an effective therapeutic approach to prevent or treat Alzheimer's," Vassar, who led the study, said in a statement.

"If people start early enough, maybe they can dodge the bullet."

Alzheimer's disease is incurable and is the most common form of dementia among older people. It affects the regions of the brain involving thought, memory and language.

While the most advanced drugs have focused on removing clumps of beta amyloid protein that forms plaques in the brain, researchers also are looking at therapies to address the toxic tangles caused by an abnormal build-up of the protein tau.

Vassar and colleagues analyzed human and mice brains to discover that a protein called elF2alpha is altered when the brain does not get enough energy. This boosts production of an enzyme that in turn flips a switch to produce the sticky protein clumps.

The finding published in the journal Neuron could lead to drugs designed to block the elF2alpha production that begins the formation of the protein clumps, also known as amyloid plaques, Vassar added.

"What we are talking about is a slow, insidious process over many years," he said. "It's so mild (people) don't even notice it, but it has an effect over time because it's producing a chronic reduction in the blood flow."

(China Daily via Agencies December 26, 2008)

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