Antibodies May Slow Alzheimer's Mental Decline

An existing treatment for immune disorders shows promise for slowing the memory decline of Alzheimer's disease.

The treatment — intravenous immunoglobulin, or IVIG for short — comes from blood. IVIG is a collection of the germ-fighting molecules called antibodies that course through healthy people's blood.

“Our very small study suggests that this already approved antibody product may be useful for treating Alzheimer’s disease,” says Norman R. Relkin, MD, director of the Memory Disorders Program at New York-Presbyterian Hospital/Weill Cornell Medical Center in New York.

Fights Sticky Brain Plaque

Reporting here today at the American Academy of Neurology 57th Annual Meeting, Relkin says that mental functioning improved in six of seven Alzheimer’s disease patients given IVIG.

The work grew out of a better understanding of the memory-robbing disorder, he tells WebMD.

In Alzheimer's disease, a sticky plaque clogs the brain. The main ingredient of this plaque is a rogue protein called beta amyloid.

Previous studies have shown that all of us make antibodies against beta amyloid. But people with Alzheimer's disease have very few of these amyloid-fighting antibodies, compared with healthy people of the same age, Relkin says.

This led Relkin and colleagues to reason that giving the antibody-rich IVIG blood product to people with Alzheimer’s disease could replenish their antibody stores.

Which is just what appears to have happened, Relkin says.

The amyloid-fighting antibodies attack and latch onto beta amyloid, drawing the proteins out of the blood and blocking the toxic burden of amyloid on brain cells, he says.

IVIG Improves Mental Function

For the study, the researchers gave IVIG to eight people with Alzheimer's disease for six months.

As expected, their brain levels of beta amyloid dropped, while their blood levels of beta amyloid antibodies shot up.

More importantly, mental functioning improved in six of the seven participants who underwent standardized testing. And it didn’t get worse in any of them.

“This is fairly dramatic as we would have expected a decline in [mental] function over six months,” Relkin says. “IVIG is helping to stabilize and even improve the [mental] status.”

The participants experienced only minor and infrequent side effects, such as chills following IVIG treatment, which is given in the vein.

A separate study in Germany, in which five patients were given IVIG, showed similar results, he notes.

Encouragement for Alzheimer’s Treatment

Together, the two small studies “give us strong encouragement,” Relkin says. But, he stresses, it’s way too soon to start treating Alzheimer’s disease patients with IVIG.

For starters, doctors don’t yet know how long a person has to stay on the treatment. And since IVIG is derived from blood of multiple donors, there’s a limited supply. The cost is high: up to $7,000 a year at the doses used in the study — about the same as dialysis for people with failing kidneys, he says.

If IVIG pans out in larger, longer studies, Relkin says he hopes to isolate the anti-amyloid antibody and use that to treat patients. “We could make a synthesized product that would be cheaper and in more ample supply,” he says.

A More Targeted Approach to Alzheimer’s

Lawrence S. Honig, MD, PhD, associate professor of clinical neurology at the Taub Institute for Research on Alzheimer's Disease and the Aging Brain at Columbia University in New York, agrees that treating Alzheimer's patients with beta amyloid-busting antibodies is a good idea.

But using IVIG — which contains millions of human antibodies in addition to beta amyloid antibodies — to treat the disease is like picking a random book off the shelf and hoping it’s the one you want to read, he tells WebMD.

Honig is getting ready to test a new compound known as AAB-001, a more specific antibody that binds to and clears beta amyloid protein from the blood.

AAB-001, which is being developed by the Elan Corporation and Wyeth Pharmaceuticals, is a synthetic, highly purified preparation of anti-beta amyloid antibodies,” he says. “This more targeted approach makes a lot more sense.”

By Charlene Laino, reviewed by Michael W. Smith, MD

SOURCES: American Academy of Neurology 57th Annual Meeting, Miami Beach, Fla., April 9-16, 2005.Norman R. Relkin, MD, director, Memory Disorders Program, New York-Presbyterian Hospital/Weill Cornell Medical Center, New York. Lawrence S. Honig, MD, PhD, associate professor, clinical neurology, Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Columbia University, New York.