Researchers at the University of California, Riverside have proposed a new explanation for how Alzheimer's disease may begin. Instead of being driven primarily by plaque buildup in the brain, the disease could start when one protein interferes with the normal function of another inside nerve cells.
For years, Alzheimer's research has largely centered on amyloid beta (a-beta), a protein that forms clumps in the brains of people with the disease. The idea gained support because inherited mutations that increase a-beta levels can cause early onset Alzheimer's.
However, despite thousands of clinical trials designed to remove a-beta, those treatments have largely failed to stop the disease or reverse its progression.
Scientists have also long known that another protein called tau accumulates in the brains of Alzheimer's patients. What has remained uncertain is exactly how tau and a-beta are connected.
"In addition to having dementia, Alzheimer's diagnosis requires both a-beta and tau buildup in the brain," said UCR chemistry professor and study lead author Ryan Julian. "But many labs focus on the role of one and ignore the other."
