Alzheimer's protein may be early risk factor
CHICAGO (Reuters) - Imaging tests may be able to detect the early signs of Alzheimer's disease long before it begins to affect memory, a finding that may lead to earlier, more effective treatments, U.S. researchers said on Monday.
They said healthy people who have an abnormal buildup of a protein in the brain linked with Alzheimer's disease have a higher risk of developing the disease.
"Our paper shows for the time that people who during life are known to have amyloid plaques in the brain - the plaques of Alzheimer's disease - have a very high risk of developing dementia in just a few years," said John Morris, director of Washington University in St. Louis, Missouri, whose study appears in the journal Archives of Neurology.
Several teams have been working on better ways to detect early-stage Alzheimer's disease in hopes of developing drugs that can fight it before it causes too much damage.
"We know that at the time when we first can detect symptoms, certain vulnerable regions of the brain are pretty damaged by the Alzheimer's pathologic process. In some brain regions at that very earliest stage, already 50 percent of brain cells have been lost," Morris said in a telephone interview.
"That made us think that trying to treat people who have the symptoms of Alzheimer's disease may not meet with much success since we are trying to treat a brain that already has substantial damage"
He said all of the treatments that have been tried or are being tested have failed so far to make a significant impact on Alzheimer's disease, a mind-robbing form of dementia that affects more than 26 million people globally.
The hope is that by finding a way to identify patients earlier, it may be possible to stage clinical trials for drugs more likely to work.
For many years, scientists have known that about a third of people in their 70s or 80s who showed no signs of having Alzheimer's disease had a significant buildup of beta-amyloid plaque in the brain, Morris said. That suggested the disease was active long before clinical symptoms showed up.
But short of an autopsy, it was difficult to find such patients.
About four years ago researchers developed an imaging agent called the Pittsburgh Compound B that let scientists use positron emission tomography, or PET scans, to detect amyloid plaques in living brains for the first time.
Morris' team used this agent to study 159 people aged 51-88 between 2004 and 2008 who started the study with no signs of cognitive impairment. Over time, 23 participants developed mild impairments, and nine were eventually diagnosed with clinical Alzheimer's disease.
A second study in 135 cognitively normal older adults aged 65 to 88, which was led by Martha Storandt of Washington University, found the level of beta-amyloid was linked to declines on memory and thinking tests over many years.
"What her study showed is people who have amyloid in the brain already are beginning to have a decline in their mental abilities," Morris said. "They don't have dementia, but they are going down hill from where they had been previously."
The studies were funded by the National Institute of Aging, one of the National Institutes of Health.
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