updated 6/20/2005 11:15:03 AM ET 2005-06-20T15:15:03

Two experimental therapies show promise at preventing a sticky gunk from clogging up the brains of Alzheimer’s patients, a buildup called amyloid that is the newest focus in the fight against the disease.

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One, an experimental drug called Flurizan, has begun late-stage testing to see if it at least helps slow Alzheimer’s inevitable worsening. Government-funded researchers are planning a large study of the second approach, a therapy called intravenous immune globulin, or IVIG.

“Most scientists think if you get rid of amyloid, it’ll moderate the disease,” explained William Thies, scientific director of the Alzheimer’s Association.

About 4.5 million Americans have Alzheimer’s, a creeping brain degeneration that slowly robs its victims of memory and the ability to reason, communicate and care for themselves. With the aging population, a staggering 14 million may have it by 2050.

No one knows what causes Alzheimer’s. But the leading theory is that something spurs abnormal production of a protein called beta-amyloid, which forms clumps that coat and then kill brain cells — plaque that is the disease’s trademark.

Healthy people’s immune systems produce antibodies that can get rid of at least some of the beta-amyloid that floats in everyone’s bodies. But older people produce one-third fewer antibodies against the protein than younger people do, said Dr. Marc Weksler of the Weill Medical College of Cornell University.

Immune globulin is a cocktail of antibodies culled from blood donors and given intravenously to treat a variety of immune-related diseases. The question is whether giving IVIG to Alzheimer’s patients might act as a sponge to soak up extra beta-amyloid.

Weksler gave eight people with mild to moderate Alzheimer’s six months of IVIG therapy. The amount of beta-amyloid in their cerebral spinal fluid — a measure of how much reaches the brain — dropped about 45 percent. Cognitive tests suggest the patients may have stabilized during treatment, although Weksler stressed that it’s impossible to tell from such a small study that had no comparison group.

“I’m encouraged but not convinced,” Weksler cautioned at an Alzheimer’s Association conference on preventing the disease. “We don’t want people to go out and buy this and treat themselves.”

But Weksler’s is the second small study to suggest IVIG may help Alzheimer’s. Now other researchers are working with the National Institutes of Health and manufacturer Baxter Pharmaceuticals, which helped fund Weksler’s work, to plan a larger study.

Myriad Genetics Inc. already has begun a large study of Flurizan, a revamped version of an old painkiller called flurbiprofen.

In Phase 2 testing of 128 people with mild Alzheimer’s, treated patients didn’t worsen as quickly as those given a placebo, with few side effects, said Dr. Gordon Wilcock of Britain’s University of Bristol. It didn’t work as well in patients with moderate-stage disease.

“If it really does work, what this drug does is reduce the rate at which beta-amyloid is made,” Wilcock said. That suggests the sooner in illness it’s used, the better.

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