The growth of plaques in the brains of people with Alzheimer’s disease comes from a failure of the brain to get rid of the plaque-forming substance known as amyloid-beta, according to a new study. This finding goes against a previous hypothesis for the plaque buildup: that patients’ brains simply make more amyloid-beta than healthy brains do.
“Clearance is impaired in Alzheimer’s disease ,” said study researcher Dr. Randall Bateman, assistant professor of neurology at Washington University School of Medicine in St. Louis.
The researchers compared a group of 12 patients who had early-stage Alzheimer’s disease with 12 healthy people of similar ages. Both groups produced amyloid-beta at the same average rate, Bateman said, but the average rate at which the substance was cleared from the brain was 30 percent lower in the Alzheimer’s patients.
At this lowered elimination rate, Bateman and his colleagues calculated, the levels of amyloid-beta seen in the brains of Alzheimer’s patients would be reached in 10 years.
The study is published this week in the journal Science.
The results have important implications for both diagnosis and treatment, the researchers said. Scientists are now interested in learning how amyloid-beta, a byproduct of normal metabolism, is moved out of the brain during breakdown and disposal. Understanding such processes in detail will be essential for researchers looking for ways to diagnose the disease before symptoms appear, and for drug developers looking to target the problems with pharmaceuticals.
Amyloid-beta was recognized long ago as a key component of the brain plaques found during autopsies of Alzheimer’s patients.
One of the ways the brain clears away the amyloid-beta normally produced by brain cells is by moving it into the spinal fluid. Studies have suggested that a drop in levels of amyloid-beta in spinal fluid is an early indicator of Alzheimer’s disease, possibly because it shows that the amyloid-beta is getting stuck in the brain and starting to accumulate there.
Treatments designed to clear amyloid-beta from the brain have recently been failing, leading some neurologists to speculate that the protein may not be causatively linked to Alzheimer’s.
According to Bateman, though, the new data associates Alzheimer’s with disruption of the brain’s ability to handle amyloid-beta normally.
“These findings support the idea that impaired amyloid-beta clearance is fundamentally linked to Alzheimer’s disease,” Bateman said.
Pass it on: The brain of someone with Alzheimer’s can’t get rid of the amyloid-beta it produces as the brains of healthy people can.
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