While there are medications that can slow—slightly--the progression of Alzheimer’s, the end inevitably comes in all those affected.

While there are medications that can slow, slightly, the progression of Alzheimer’s, the end inevitably comes to all those affected. New data suggests that Immunoglobulin, used to treat multiple sclerosis patients, could work in Alzheimer’s patients as well.

Immunoglobulin contains antibodies against a protein thought to be a main suspect in Alzheimer’s disease. That protein, called beta-amyloid, causes the formation of protein deposits which can damage and destroy sensitive nerve cells, leading to the early senility of Alzheimer’s.

In the study of five patients, this drug, IVIG, given intravenously every four weeks over six months, lowered the levels of the beta-amyloid protein in the fluid around the brain by more than 30 percent.

Dr. Mark Mehler, Chairman of the Department of Neurology at Montefiore Medical Center, New York, says, “There’s evidence from other diseases that the pathology is on going. And there is some hope that if you could reverse part of the pathological process before the cells actually die, you may be able to intervene even late in a disease. But there is also a lot of evidence because theses diseases are biologically complex, that if you intervene late the chance of you effecting either a cure or a significant retardation of the progression is little. That’s the problem.”

The researchers also found four of the five patients actually improved slightly on mental status tests…none deteriorated over the six month period. Still, Dr. Mehler thinks this would only be a disease halting approach, not one that can reverse the problem.
“The only way you’re really going to cure the disease is to re-establish the neuro-networks that have been damaged in the disease. And probably the only way that you can do that and effectively in the future is through stem-cells. So I think that research in these fields really needs to happen because it’s really become an epidemic.”

There is a lot of controversy in the field as to whether or not these beta-amyloid plaques are just the by-product of the disease or if the plaques are central to the problem. That still to be worked out, but this research gives a small boost to support the thinking it does indeed contribute to the disease.

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