Why We Age: Molecular Link to Alzheimer's and Parkinson's Dr. David J. Demko, gerontologist AgeVenture Syndicated News Service 07-12-05 Anti-aging research intends to help people live longer by addressing two types of human aging. The first, primary aging, refers to the origin of the aging process. Break this "primary aging" code, and humans just might live 600 to 800 years and beyond. The other type of human aging refers to "secondary aging", diseases which occur in late life. Break the "secondary aging" code and chronic diseases will be eradicated, allowing humans to live 120 years, which is the scientifically established "maximum life span" for humans. Today, I'm reporting on a major breakthrough in secondary aging. International researchers have discovered a common link between Alzheimer's and Parkinson's disease. This team of chemists and molecular biologists discovered a process that explains why humans are at risk to Alzheimer's and Parkinson's. The focus of this breakthrough research lies deep within the human cells, specifically, the molecular level of secondary aging. Within human cells, you will find microscopic, rope-like structures called amyloid fibrils. These fibrils are formed by protein molecules which are linked together in a water-rich environment that allows the molecules to function normally. Here's the problem. Sometimes these protein molecules are forced to exist in a dehydrated environment. David Eisenberg, a UCLA member of the research team, explains this dehydrated state as caused by a "molecular zipper", creating an unhealthy environment for protein molecules to function as needed. According to Eisenberg and his colleagues, the "molecular zipper" refers to an amyloid fibril (protein) in which the water is squeezed out and "zipped up". There lies the problem, because water is essential to the normal functioning of protein (amyloid fibril) molecules. The challenge now is to understand how the water-tight zipper fosters Alzheimer's and Parkinson's disease. Understanding this process may provide a rational basis for developing drugs to fight these diseases, says Melinda Balbirnie, a UCLA member of the research team. Eisenberg and his colleagues believe that Alzheimer's and other fatal "amyloid fibril" diseases have proteins containing the "molecular zipper", that dehydrates the protein molecules. If scientists can understand how "molecular zippers" form, they may develop a strategy to reverse or prevent the dehydration process. The researchers believe the proteins associated with Alzheimer's and other amyloid fibril diseases are "transformer" proteins that instead of doing their normal work, change to a diseased state associated by the dehydration process. The research was funded by the National Institutes of Health, the National Science Foundation and the Howard Hughes Medical Institute. See related articles in AgeVenture archives. AgeVenture Headline News AgeVenture Lifestyle Features AgeVenture News Service, www.demko.com BACK TO TOP