Memory lapses are one of the first clues. As the disease progresses, victims get lost in their own neighborhoods and even in their own homes. Unaware of what is happening, they regress to a childlike state, bringing anguish—and constant anxiety—to their families. Eventually, the patients lose control over their bodies and lie curled up in bed. So far, there is no cure for Alzheimer’s disease and precious little that can be done for the estimated 160,000 mostly elderly Canadians who suffer from it, other than to care for them with compassion. Now, following a series of research breakthroughs, scientists have begun to look at Alzheimer’s disease in new ways and to lay the groundwork for effective treatments that could emerge by the end of the century. Dr. Ivan Lieberburg, vice-president in charge of Alzheimer’s research at San Francisco’s Athena Neurosciences Inc., a biotechnology company, predicts that “there will be therapies almost certainly by the year 2000—treatments that will really slow or alter the course of Alzheimer’s.”
The quickening research pace was certain to be a dominant theme at a conference in Toronto this week of organizations from 30 countries representing health-care professionals and the families of Alzheimer’s victims. In one thrust, scientists during the past three years have begun to track down genes that apparently play a role in Alzheimer’s. Though the disease probably has more than one cause, knowing which genes are involved is almost certain to yield understanding of—and eventually ways of treating—a baffling disease. At the same time, a Vancouver chemist and physician, Dr. Pat McGeer, and his American partner, neurobiologist Joseph Rogers of the Sun Health Research Institute in Sun City, Ariz., have challenged orthodox thinking about Alzheimer’s by suggesting that an attack by a patient’s own immune system may be responsible for killing brain cells.
In a test carried out among 28 Alzheimer’s victims last year, McGeer and Rogers showed that treating them with an Aspirin-like compound called indomethacin that reduces inflammation resulted in a slight improvement in the mental ability of Alzheimer’s patients. In a control group, patients who did not receive the drug continued to decline. While some researchers say that it is too early to evaluate the work of McGeer and Rogers, others say that the two men may have opened an important avenue of research. “It’s very exciting, very promising,” says Zaven Khachaturian, director of Alzheimer’s research at the U.S. National Institute on Aging in Bethesda,
Md. “Their theory deserves to be tested more widely.”
McGeer and Rogers began collaborating eight years ago, after Rogers found evidence of immune system activity in the brains of Alzheimer’s victims and wondered what role that might play in the disease. When Rogers discussed his findings at a 1986 meeting of the American Society for Neuroscience in Dallas, he recalls, “McGeer was really the only one who paid any attention.” McGeer, who was leader of the tiny B.C. Liberal Party from 1968 to 1972 and served as a Social Credit cabinet minister during the 1970s and 1980s, went back to his laboratory, where he found evidence to support Rogers’s findings.
The two men subsequently formulated a new theory about Alzheimer’s. In their hypothesis, the disease involves an inflammatory condition created when the brain’s immune system is activated and begins attacking and killing brain cells. The actual killer is a part of the immune system called the complement system cascade; its normal function is to amplify the effects of antibodies created to fight off invading bacteria or viruses. In the brain of an Alzheimer’s patient, says McGeer, the cascade is “activated not by invading organisms, but by elements in the Alzheimer brain.” McGeer and Rogers think that they have identified one of the factors involved in v triggering the deadly over| heating: a protein called £ beta-amlyoid, whose func% tion is unknown.
“ Other scientists think that beta-amyloid itself is the principal killer of brain cells. Two years ago, British scientists established a link between the genetic region in cells that produces beta-amyloid and families afflicted with the relatively rare early-onset form of Alzheimer’s, which can strike people in their late 20s.
Some U.S. and Canadian researchers are focusing on another suspected Alzheimer’s villain—a tiny protein known as APOE (for apolipoprotein E) that is responsible for ferrying cholesterol through the bloodstream. In August, scientists at Duke University Medical Centre in Durham, N.C., reported that in a study of 234 people with a family history of late-onset Alzheimer’s, 64 per cent carried a version of the gene called APOE4. Other studies, including one by University of Toronto scientists (carried out in conjunction with the Duke University scientists), confirmed the apparent link between Alzheimer’s and the APOE4 gene. According to Peter St George-Hyslop, the neurologist in charge of the Toronto study, more than half of all Alzheimer’s cases may involve people who carry the APOE4 gene.
Meanwhile, Rogers and McGeer have launched another, larger trial, in which about 100 Alzheimer’s patients in the Sun City area are being treated with anti-inflammatory drugs. Their hope: that the test will support their earlier findings by slowing the effects of Alzheimer’s. There have been many proposed treatments for Alzheimer’s, says McGeer, but so far “no one has come up with any ideas that will stop neurons [brain cells] from dying. And that’s got to be the objective.” As scientists explore new approaches to Alzheimer’s disease, the chances of realizing that objective have never looked better.
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