After the widely publicized failure of a potential vaccine for Alzheimer's disease in 2002, new hope may be on the horizon.
According to research presented Wednesday at the 10th International Conference on Alzheimer's Disease and Related Disorders in Madrid, Spain, researchers are already making great strides in developing a vaccine for this progressive brain disorder.
Affecting about 4.5 million Americans, Alzheimer's disease gradually destroys a person's memory and ability to learn, reason, make judgments, communicate, and carry out daily activities, according to the Alzheimer's Association.
Alzheimer's disease is a result of damage to nerve cells in the brain. Plaques of a protein called beta amyloid contribute to the damage and death of brain cells. The antibody therapy tested in this study targeted beta-amyloid protein and amyloid plaques.
The older trial was halted in 2002 when 6% of participants developed a dangerous brain inflammation called encephalitis; some also developed brain shrinkage. But two new approaches toward vaccines seem to avoid such problems, explains John C. Morris, MD, director of the Alzheimer's Disease Research Center of Washington University in St. Louis.
One promising approach is known as passive immunization. In a nutshell, a vaccine helps your body create antibodies to fight off disease. An active vaccine marshals the body's own disease- fighting mechanism to attack the disease. By contrast, a passive immunization strategy is based on treating patients with antibodies that are manufactured.
"This is a different way to grow antibodies," Morris explains. "We grow them in test tubes and give them to patients so the patient can then launch an immune response, but since the body is not generating the antibodies on its own, they will not overstimulate their immune system."
Currently there are two trials in different stages looking at this approach, Morris says.
In one new study presented here, researchers including Eric Seimers, MD, from Eli Lilly and Company of Indianapolis, gave 19 people with Alzheimer's disease an intravenous (IV) infusion of one of four doses of antibodies over a half hour. Side effects were similar across all dosage groups, but in the highest-dose group, people reported mild shaking and dizziness that lasted less than two hours after the infusion.
Although there were no changes in mental function among participants, the researchers noted changes in the blood levels of beta-amyloid.
"It's possible that the optimal effects would be to introduce vaccines at a time when the changes are just beginning," he says. "It's conceivable that if we detect changes by imaging even when there is substantial memory loss, disease-modifying therapies, such as passive vaccines, will have the most benefit," Morris says.
In addition to passive immunization, newer, more targeted vaccines do not seem to have the same side effects as the older vaccines. "Some researchers are working on a more specific vaccine that if given to people will cause antibodies to attack amyloid plaques and will not have inflammation as a side effect," he says.
The good news is that "we are now testing treatments that if found to be safe and effective will have the chance to halt the disease process, and we are on the cusp of early detection of Alzheimer's with novel imaging technologies," he says. "Putting the two together is the way to go particularly as baby boomers reach age 65."
Gleaning his crystal ball for WebMD, Morris says, "Alzheimer's is complicated and I would be delighted if we could have one or more new effective therapies by 2020."
SOURCES:: 10th International Conference on Alzheimer's Disease and Related Disorders, Madrid, Spain. July 15-20, 2006. John C. Morris, MD, director of Alzheimer's Disease Research Center of Washington University, St. Louis.
By Denise Mann
Reviewed by Louise Chang, M.D.
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