HealthSCOUT - August 05, 2004
In another promising development in Alzheimer’s research, research in mice suggests that a drug treatment can halt the progression of the disease in its early stages.
Tests of the drug in humans were discontinued because of dangerous side effects. But a neuroscientist said the antibody-based drug still holds plenty of promise, especially considering that researchers continue to prove its worth.
"There’s a series of studies that suggest we may well be able to slow the disease using this approach," said Michael Hutton, a professor of neuroscience at the Mayo Clinic College of Medicine in Florida.
Alzheimer’s disease affects an estimated 4.5 million Americans, and the number is expected to grow as baby boomers become senior citizens. The best current treatments only delay the disease for about six months, Hutton said, leaving patients to decline into forgetfulness, behavioral problems, inability to speak, and other devastating symptoms.
The disease begins when pieces of gunk called beta-amyloid plaques develop in the brain. Then, neurofibrillary tangles appear in neurons. Both the plaques and the neurons kill off brain cells, leading to declines in mental function.
In the new study, researchers from the University of California at Irvine transferred defective genes from humans to about 30 mice to give Alzheimer’s disease to the animals, which normally don’t get it.
Just like humans, the mice start to forget things. Scientists test their memory by dumping them into tiny swimming pools and checking to see if they remember where to find platforms that allow them to get out of the water, said study co-author Frank LaFerla, an associate professor of neurobiology and behavior.
After the mice developed the early stages of Alzheimer’s, scientists treated them with antibodies -- a kind of immune system soldier -- designed to seek out and destroy the plaques.
The researchers discovered that the treatment, if done early, removed both the plaques and the tangles, suggesting the two are closely linked.
The findings, which appear in the Aug. 5 issue of Neuron, appear to confirm a theory that plaques lead to tangles, LaFerla said. It also spells hope for patients who haven’t developed many problems on the tangle front. "What that means is the earlier you treat a patient with Alzheimer’s disease, the better your chances for success."
But this spells trouble for people who are in the later stages of the disease and may be stuck with stubborn tangles. "We now also have to consider therapies that are aimed at removing or busting up the more advanced tangles," LaFerla said. "We’ll have to find tangle busters as well."
There are several caveats to the research. It’s in mice, not humans, and it’s hard to study exactly what is going on in the brains of humans until after death. In fact, there’s no way outside of an autopsy to confirm that someone even has Alzheimer’s disease, although Hutton said doctors do a pretty good job of diagnosing it.
Then there’s the matter of side effects of the antibody treatment. A previous study of an Alzheimer’s vaccine had to be halted because some patients developed potentially fatal swelling of the brain.
But LaFerla is hopeful. "We’re all on the right road," he said. "It’s now about finding the right exit."