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---------------------------------------------------------------------------- Researchers report advances in understanding Alzheimer's ---------------------------------------------------------------------------- Copyright 1997 Nando.net Copyright 1997 St. Petersburg Times (July 22, 1997 2:15 p.m. EDT) - The shadowy, complex causes of Alzheimer's disease continue to come into focus as a research team reports that a toxic protein associated with the disease damages blood vessels. The University of South Florida team also found that an antioxidant prevented the damage in laboratory rats, a finding that supports other recent research that showed antioxidants like vitamin E and anti-inflammatory drugs like ibuprofen might slow Alzheimer's relentless destruction of brain cells. The study was reported Monday in an academic journal that deals with submicroscopic cellular analysis. The team is working in an area of Alzheimer's research that has gathered lots of headlines in recent years. The issue is whether blood supply to the brain and cellular damage that releases toxic substances known as free radicals, ultimately results in Alzheimer's. If the researchers are correct, it suggests that preventing the damage to cells and blood vessels could decrease the chance a person might get Alzheimer's. More than 4-million Americans have the disease, which slowly saps memory and later destroys all mental and physical functions. "We believe (the study) will provide a rapid, valuable method for testing drugs to prevent or treat Alzheimer's," said Dr. Tom Thomas, the study's lead investigator who recently left USF for private practice. As always, researchers urge caution. Alzheimer's is a puzzling disease whose exact cause is unknown and whose treatments are evolving swiftly on several fronts. But a growing body of evidence suggests the disease might be the result of an interaction of genetic and environmental causes, similar to heart disease and other disorders associated with aging. Researchers know certain people with particular genes are more likely to get the disease. But is their chance -- and the chance of others without the genetic markers -- higher if diet, stroke, other diseases, environmental toxins and other factors cause cellular and blood vessel damage? That's the area Thomas and his colleagues are pursuing. "The key to the start of Alzheimer's may be the breakdown in blood vessels," said Dr. Johannes Rhodin of USF, who developed the equipment used to view the arteries and capillaries through the thin membrane of the rats' abdomens in this study. "That would make it possible for the toxic protein to leak out and trigger an inflammatory response that kills nerve cells." Thomas and his colleagues injected beta amyloid, a protein found in clumps in the brains of Alzheimer's victims, into live rats. They wanted to see the reaction, suspecting the protein would damage the arteries and blood vessels, as had occurred in their earlier research in a test tube. Using special microscopic videotaping equipment and later an electron microscope, researchers found that beta amyloid damaged the lining of the arteries and eventually broke through blood vessel walls. That's a sign of an inflammatory response similar to what happens in rheumatoid arthritis. The researchers also tested an antioxidant normally found in cells to see if it would prevent the damage. They suspected the beta amyloid protein was causing the release of free radicals, a chemical that occurs normally in cell metabolism, but that in too large a quantity damages and kills cells. Anti-oxidants, which also occur naturally in our bodies and in certain vitamins like E, destroy free radicals. The USF team -- Thomas, Rhodin and Truitt Sutton and Margaret Bryant -- found the anti-oxidant, known as superoxide dismutase prevented the vascular damage in rats. This finding supports recent research that found Alzheimer's patients were healthier and lived longer after receiving large doses of vitamin E each day. Despite the encouraging findings, Thomas stressed that much more research is needed. "It is a long process that can take years," he said. The USF team next plans to look at the reaction of beta amyloid in the brains of living rats. No one should go out and start popping vitamin E or ibuprofen, Thomas warns. Those substances in large quantities can have dangerous side effects. There are two drugs, called Cognex and Aricept, on the market that improve symptoms of Alzheimer's by slowing the breakdown of a neurotransmitter in the brain. Other drugs are being tested, including anti-inflammatory drugs and drugs that try to slow cellular damage. "We are moving closer," said Dr. Mildred V. "Mimi" Farmer, medical director of Clinical Studies, which conducts drug tests for Alzheimer's and other diseases in St. Petersburg and other cities. "But it is also a chicken-and-the-egg question: What is a cause and what is a symptom?" Is blood vessel damage leading to cellular breakdown that kills brain cells and causes Alzheimer's, as the USF team suspects? Or is such damage the result of other factors that are causing the disease? It could be both, researchers say. Alzheimer's may be resulting in several ways from a variety of genetic and lifestyle factors, meaning that some combination of current drugs is the solution. "It is," Thomas said, "an exciting time." By JOHN A. CUTTER, St. Petersburg Times ---------------------------------------------------------------------------- <http://www.nando.net/newsroom/ntn/health/072297/health21_3603.html>