After years of setbacks, Alzheimer’s researchers are sounding optimistic again. The reason: a brain protein called tau.
At this year’s Society for Neuroscience meeting in Washington, D.C., there are more than 100 papers on tau, which is responsible for the tangles that form in the brains of people with Alzheimer’s. In the past, tau has received less attention than another protein called amyloid beta, which causes the sticky plaques associated with Alzheimer’s.
“Many people focused on amyloid beta for many years,” says Julia Gerson, a graduate student in neuroscience at the University of Texas Medical Branch, who presented a paper on tau at the neuroscience meeting. “Now it’s coming out that tau might be more important.”
“Clearly both are working together, conspiring if you will, to bring down cell functions and cell survival over the years as the disease unfolds,” says Dr. Lennart Mucke, a neurologist who directs the Gladstone Institute of Neurological Disease, a research center affiliated with the University of California, San Francisco.
In the past decade, several promising drugs that merely lower amyloid have failed to stop Alzheimer’s. Those failures, Mucke says, helped persuade scientists to take a closer look at tau, which has produced some surprising findings.
“Initially it was thought that tau was purely inside brain cells,” he says. “But now we recognize that it can actually exist outside of cells and even transfer from one cell to the next.”
The idea that tau can spread from cell to cell like an infection suggests a new way to treat Alzheimer’s, Mucke says. “If we could figure out how to stop that spread, maybe one could limit the disease to just some brain regions, instead of having it go everywhere.”
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