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UC San Diego Researchers Answer Key Alzheimer’s Question

Evening Edition

Aired 8/12/13 on KPBS Midday Edition.


Subhojit Roy, Associate Professor Pathology & Neurosciences, UC San Diego

Dr. Maria Carrillo, Vice President, Medical and Scientific Relations for the National Alzheimer's Association


Researchers into Alzheimer's disease have puzzled for some time about why previously healthy brains develop the disease.

Scientists can now measure abnormal proteins in the brain called amyloid beta...
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Above: Scientists can now measure abnormal proteins in the brain called amyloid beta. Excessive accumulation of this protein (as seen bottom right) is one of the hallmarks of Alzheimer's disease. Researchers hope to use brain scans to study whether intervention — such as a cholesterol-lowering drug — may help prevent a build-up of amyloid beta decades before the disease may develop.

As it turns out, we all have the same ingredients in our brains that can lead to the development of Alzheimer's. So why don't we all get it?

A research team at UC San Diego School of Medicine asked that question and their study produced some intriguing results.

Associate Professor of Pathology and Neurosciences at UC San Diego, Subhojit Roy said he discovered a trick of nature in most people that separates a protein from an enzyme that when combined triggers Alzheimer's disease.

"It’s like physically separating gunpowder and match so that the inevitable explosion is avoided,” he said

“Knowing how the gunpowder and match are separated may give us new insights into possibly stopping the disease.”

Roy and his team found that when a protein, called amyloid precursor protein (APP) comes together with an enzyme called beta-secretase or (BACE), they produce beta-amyloid protein, triggering a sequence of events that leads to impaired cell function and death.

But that doesn't happen in people with healthy brains.

“Nature seems to have come up with an interesting trick to separate co-conspirators,” said Roy.

Roy said these results are significant because they can lead to a new approach to fighting Alzheimer's.

“An exciting aspect is that we can perhaps screen for molecules that can physically keep APP and BACE-1 apart,” said Das. “It’s a somewhat unconventional approach.”

Alzheimer's is by far the most common form of dementia. Five million Americans live with the disease and that number is expected to triple by 2050.

Roy and colleagues published their findings in a paper in the August 7 issue of medical journal Neuron.

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