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Antibody holds hope for Alzheimer's, USF study finds
By STEPHEN NOHLGREN, Times Staff Writer
University of South Florida scientists have discovered an antibody that seems to reduce two tell-tale characteristics of Alzheimer's disease. The antibody has been tested only in mice. Human applications are several years away. While promising research often runs into snags and dead ends, the USF findings still are "quite exciting," said Zaven Khachaturian, senior medical adviser for the Alzheimer's Association of America. "It gives us a new approach for dealing with two of the leading ideas in terms of the pathology of the disease." The findings, published Monday in the online journal Nature Neuroscience, follow several years of research at USF's Roskamp Institute into the brain's immune system and its relationship to Alzheimer's. When pathologists inspect brains ravaged by Alzheimer's, they find bits of protein called amyloid clumped together in sticky plaques. The surrounding tissue is inflamed, indicating that the brain's immune cells have attacked something. The pathologists also find remains of dead neurons, the cells that form memory. Both amyloid plaques and inflammation are suspected as culprits that may kill memory cells. That's why anti-inflammatory drugs like ibuprofen might have a significant preventive effect. There are two theories about how the plaques and inflammation relate. The amyloid plaques may kill neurons directly, and the inflammation is just a byproduct, said Harvard neurologist Rudy Tanzi. Or perhaps, the immune system sets out to attack the amyloid with inflammation but kills healthy memory cells in the process. "It could be like friendly fire," Tanzi said. "The brain's immune system is very primitive. The immune cells send out free radicals and shoot everything in sight." The Roskamp tests addressed both theories by disabling the immune system's trigger. The brain's immune cells, called glia, have receptors on their cell wall that wait for signals to attack and clean up foreign substances. About a year ago, Roskamp researchers began injecting 8-week-old mice with an antibody that blocked the glial receptors from receiving signals, said Dr. Jun Tan, lead author of the study. These were not just any mice. They were genetically engineered to develop raging Alzheimer's at a young age. Every 10 days, the mice got another shot of antibody. Then, at 8 months, they were killed so their brains could be examined. They had 60 percent fewer plaques than control mice that didn't receive the injections. And their brains were not as inflamed. "This is more exciting than the average Alzheimer's (research) story," Tanzi said. "It implicates a specific target," meaning the immune cell's receptor. "That means drug companies can look at this paper and think, maybe we should target this receptor with drugs." The antibody, called the anti-cd40L anti-body, is already being tested in humans as a possible treatment for multiple sclerosis, said Tan. Most likely, it wouldn't be used directly for treatment of Alzheimer's because it's a large protein that may be difficult to deliver directly to the brain. Now that it might be useful, however, drug manufacturers could try to develop a chemical that would mimic it and block the immune system receptors in the same fashion. Like other parts of the body, the brain needs an immune system. The idea would be to adjust chemical levels enough to mute the immune system without shutting it down altogether. "These are all speculations and possibilities at this stage," Khachaturian said. "Families need to recognize that developing therapies is a tricky business. It's a long way from studies in mice before you get a molecule that works in humans. "Still, we need to be optimistic. Every time we have another option to developing treatment, that's good news."
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