A break-through in Alzheimer's research has found a compound that blocks the progression of Alzheimer's disease. The discovery occured at the University of California at Irvine. An Alzheimer's research group there has announced the new Alzheimer's drug treatment that they have named AF267B. In tests on mice AF267B reversed the symptoms of memory loss and problems with learning that are associated with Alzheimer's disease. The drug is not a cure for the disease, but it is important because the research has shown that it will block the progress of Alzheimer's. That means that once diagnosed it appears that the loss of brain function can be controlled. Prior research indicated that protein clumps and tangles were often found in the brains of those suffering Alzheimer's AF267B reversed those symptoms. The new drug was designed to activate receptors for a brain chemical called acetylcholine. Acetylcholine receptors are abundant in the cortex and hippocampus of the brain. Both of these receptors are known to be vulnerable to the build-up of the protein plaques and tangles that are evident in the brains of Alzheimer's patients. They are believed to destroy brain cells. The U.C. researchers first engineered mice to show classic signs of Alzheimer's. These mice were then treated with AF267B. After treating the animals with the new Alzheimer's disease medication the mice were better at learning and memory improved. AF267B appears to mimic the action of acetylcholine, binding to its receptors and boosting levels of enzymes involved in breaking down the key protein that forms clumps and tangles in brain cells. In the words of team research leader Professor Frank LaFerla: "AF267B could be a tremendous step forward in the treatment of Alzheimer's disease. Not only does it appear to work on the pathology of Alzheimer's and ease its symptoms, it crosses the blood-brain barrier, which means it does not have to be directly administered to the brain, a significant advantage for a pharmaceutical product." This Alzheimer's research builds on earlier studies and has allowed the U.C. scientists to overcome some of the problems seen in previous strains of AF267B. Prior problems included unacceptable safety margins and a higher potential for side-effects. It is very encouraging news that the drug was able to reduce some of the amyloid plaques and tangles in areas of the brain particularly affected by Alzheimer's - the hippocampus and cortex. It is acknowledged that the new Alzheimer's drug treatment is not the final solution for the disease. More research will be needed to improve the drug's effectiveness, to ensure it is safe and to prove it can produce the same results in humans. |
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