Amyloid-β Removal Studies Might Lead to New Alzheimer’s Disease Drug Discoveries

Amyloid-β Removal Studies Might Lead to New Alzheimer’s Disease Drug Discoveries
Two studies from the Washington University School of Medicine in St. Louis, Missouri, reveal new insights into amyloid-β — the plaque-forming protein scientists believe is at the root of Alzheimer’s disease. Both studies homed in on the removal of amyloid-β from the brain, a process thought to be defective in Alzheimer’s patients, offering up new clues on how to prevent the protein from aggregating in the brain. Scientists have never been able to ascribe a function to the amyloid-β protein, and most people believe that it is released from brain cells as a byproduct of normal brain activity. Although alternative theories have emerged during recent years depicting amyloid-β as an antimicrobial factor crucial for our immune defense against infections, a defective removal of the protein from the brain might lie behind its accumulation in the brain, a phenomenon scientists believe leads to Alzheimer’s disease. Measuring changes of amyloid-β in the brain allows researchers to explore the effects of drugs intended to lower brain levels of the protein, but until now, available methods have been crude, allowing measurements within a one-hour window. "For the last 14 years we had a technique in which we would do something to the mouse – give it a drug, have it perform a certain behavior – and we'd find out what happened to its amyloid beta levels an hour later," said John Cirrito, senior author of one of the studies. "Waiting that long just wasn't good enough. Neural activity happens on
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