Scientists studying the brains of mice have discovered how the toxic protein that destroys the brain cells of Alzheimers patients enters the brain. When the researchers gave mice a drug that blocked the process, flow of the protein into the brain was virtually halted and existing accumulations of it in the brain plummeted by more than 70 percent. The results of the research will be published in the July 1 issue of Nature Medicine.
The new findings center on amyloid beta, a tiny protein molecule that accumulates over time to form tell-tale plaques in the brain tissue of Alzheimers patients. While various cells within the brain itself produce amyloid beta, that amount may be just the tip of the iceberg. Mounting evidence suggests that the bulk of amyloid beta is produced in cells throughout the body and gets circulated in the blood. The new study reveals for the first time how the protein gets from the blood into the brain, thwarting the brains elaborate filtration mechanism that normally keeps away toxins. In mice that had been genetically engineered to develop Alzheimers, the process ran wild, pouring amyloid beta into the brain at eight times the rate of healthy mice.
"For more than a decade weve known that this protein wreaks havoc in the brains of Alzheimers patients, but we havent known how it gets there or how to prevent it from getting there. This study answers both of those basic questions, and opens an entirely new avenue for the treatment of Alzheimers disease," said lead author Berislav Zlokovic, M.D., Ph.D., of the University of Rochester Medical Center.
Christopher DiFrancesco | EurekAlert!
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The Max Planck Institute for Physics (MPP) is opening up a new research field. A workshop from November 21 - 22, 2016 will mark the start of activities for an innovative axion experiment. Axions are still only purely hypothetical particles. Their detection could solve two fundamental problems in particle physics: What dark matter consists of and why it has not yet been possible to directly observe a CP violation for the strong interaction.
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