ESCAPED an enzyme? These plates characteristics can accumulate in the brains of some people with Alzheimer's disease
because an enzyme can not break b amyloid.
SAN DIEGO - When you hear of insulin, you probably think of diabetes, but perhaps it could soon bring to mind the disease Alzheimer. The connection is an enzyme that breaks insulin and a protein that causes Alzheimer's disease. Now, a preliminary study suggests that dysfunction of this enzyme may be responsible for Alzheimer's disease in some families.
Alzheimer patients suffer from excessive amounts of a protein called b amyloid, which for some reason built into their brain. In some cases, it appears that genetic mutations increase the production of b amyloid. Alternatively enzymes - so far unknown - which break b amyloid simply do not work fast enough. In 1994, researchers found the first candidate: Insulin-degrading enzyme (IDE) breaks down b amyloid in a test tube. FDI but does not seem likely to be clinically important, because it is normally found in the cytoplasm, and b amyloid built between the inner closed cells or vesicles in the cell.
New evidence for the importance of FDI came from Dennis Selkoe, Wesley Farris and colleagues from Harvard Medical School in Boston. Although screening of brain cells to proteins that destroy b amyloid, they discovered that FDI seemed to have more naturally secreted b amyloid. At the annual meeting of the Society for Neuroscience here Farris November 11 reported that blocking FDI activity stopped approximately 70% of b amyloid ventilation in isolated cell membranes from brain tissue. And causing cells to overproduce FDI intensified the rate of b amyloid ventilation.
The team also worked with the geneticist Rudolf Tanzi and his colleagues from Massachusetts General Hospital to see whether mutations in the gene for FDI could contribute to Alzheimer's disease in people with a family history of disease. The Tanzi group provided data on the seven families of Alzheimer's disease appears to be related to the region of chromosome 10 that contains idea. Selkoe's team analyzed the cells of these families and found that members of the same family had significantly fewer b amyloid degradation than normal, suggesting that FDI can contribute to broken disease. The team is looking for more families with Alzheimer's disease that can have such mutations.
The data are "very encouraging," says Alzheimer's researcher Frank Laferla of the University of California, Irvine, but he remains convinced that IDE cleans most of b amyloid . "It will not be a single enzyme that degrades b amyloid," he said.
Related Sites
Summary of the Society for Neuroscience meeting
learn more about Alzheimer's disease from the National Institute on Aging
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