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Early in April, the first of a fleet of environmental monitoring satellites will lift off from Europe's spaceport in...
Since 2000, U.S. government health research agencies have spent almost $1 billion on an effort to churn out thousands...
Magdalena Koziol, a former postdoc at Yale University, was the victim of scientific sabotage. Now, she is suing the...
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Considered an icon of conservation science, researchers at World Wildlife Fund (WWF) headquarters in Washington, D.C.,...
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Alzheimer's Gene Accelerates Multiple Sclerosis
15 February 2001 7:00 pm
Two seemingly unrelated diseases---Alzheimer's and multiple sclerosis---have been found to share a troublesome gene. APOE4, a gene that predisposes people to Alzheimer's, is now shown to predict how quickly and severely multiple sclerosis progresses. The connection could yield insights into how both diseases damage the brain, and possibly inspire new treatments.
Multiple sclerosis is caused by the destruction of myelin, a fatty substance that surrounds and insulates nerve fibers. The disease disrupts nerve signals and impairs movement, coordination, vision, and sometimes thinking. Although the ultimate cause of multiple sclerosis is a mystery, some studies have suggested a role for APOE genes. These genes produce proteins that transport fats and somehow help repair damaged neurons. APOE4, the form of the gene linked to Alzheimer's, appears to be less efficient than other APOE genes at enabling this repair.
The new study, headed by neurologist Amos Korczyn of Tel Aviv University, Israel, is the first to demonstrate that APOE4 determines the course of multiple sclerosis. The team studied 205 patients and assessed how their disabilities had progressed, in some cases over the past 40 years. When they sorted the patients according to which form of APOE they carried, they found that people with APOE4 on average got multiple sclerosis about 3 years earlier than usual, had a more precipitous decline in health, and had more severe cases of the disease, the researchers report in the 13 February issue of Neurology.
"This is a great advance for the field," says neurologist Hans Hartung of the University of Graz, Austria. "It's the most comprehensive study to date, with the lengthy follow-up adding much [credence] to the data." He also agrees with Korczyn, who says, "once we know more about what APOE does with respect to nerve regeneration, pharmaceutical companies can try to simulate these actions with drug therapy." But, as Korczyn points out, that may be far in the future.