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More than a century after German psychiatrist Alois Alzheimer first lectured about the gooey mass of plaques and tangles he noted in a postmortem brain tissue sample, scientists are still debating what causes Alzheimer's disease.
The majority of scientists have agreed that plaques result from overproduction of beta-amyloid -- a protein found in the cell membrane of neurons. In people with Alzheimer's, this protein accumulates in clumps between brain cells.
But recently, researchers from Washington University in St. Louis arrived at a new theory: that rising brain levels of beta-amyloid do not mean that patients are making more of it but that they can no longer clear it from their brains as effectively.
The study. As reported in the journal Science, the investigators tested 24 people, average age 74, and separated them into a group composed of people with minor Alzheimer's disease and another whose members were cognitively normal. Special testing revealed that both groups produced beta-amyloid at the same average rate within the brain.
The study subjects were then tested to see how the beta-amyloid was cleared from their brains. One of the ways the brain does this is by moving it to the spinal fluid for disposal. The researchers took samples of cerebrospinal fluid by inserting a needle into the subjects' backs and drawing off the fluid that normally surrounds the spinal cord. They found that those with Alzheimer's had decreased clearance of beta-amyloid from the brain to the cerebrospinal fluid -- about 30 percent less than those who were cognitively normal. This suggests that Alzheimer's is associated with disruption of the brain's ability to normally handle the beta-amyloid.
What it means. Early diagnosis of Alzheimer's has been elusive. But because researchers have uncovered a possible mechanism of early disease development, it is possible that this discovery could lead to both a test for early detection and the development of effective therapies to stop or reverse Alzheimer's memory disruption. They calculate that it would take an adult 10 years to build up enough amyloid in his or her brain to reach the amount typically present in someone with Alzheimer's.
This knowledge could offer doctors a window of opportunity to diagnose someone long before dementia symptoms develop. Once they learn they are at risk for dementia, people could make more concerted efforts to reduce their personal risk factors for Alzheimer’s. At the same time, pharmaceutical companies could work on targeted medications to halt brain damage before symptoms become irrevocable.
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