Will it exacerbate Alzheimer's disease? Animal studies similar to the treatment of human Alzheimer's disease indicate that the treated antibodies may actually be harmful.
Antibodies in human clinical trials have been found to destroy the sticky plaques that form in the brain. In mouse models of Alzheimer's disease, antibodies also seem to be more able to activate brain cells and eventually stop functioning.
"We think this may be the mechanism by which these antibodies failed in human clinical trials," said Marc Busche of the Technical University of Munich, Germany.
Busche and his colleagues used the same antibody drugs in mice that mimic Alzheimer's disease and normal mice. After treatment, they found that the brain cells of diseased mice were five times more active than normal mice.
Amyloid plaque rupture
When amyloid plaques in Alzheimer's disease are formed, fragments called β-amyloid aggregate. Busche et al. previously discovered that β-amyloid protein can cause neuronal hyperactivity. They believe that when antibodies destroy these plaques, their effect is worse than when the plaques remain intact.
After many failures in the process of trying to treat Alzheimer's disease, drug developers began to try to detect and treat Alzheimer's disease as early as possible.
So Bushe and his team studied the effect of the drug in the early stages of Alzheimer's disease in these mice. At this time, there are no plaques in the brain, neurons become more active, and the condition worsens. Symptomology.
The mouse may mislead us
"We found that even very young mice were active before the plaques were deposited. It is not yet clear what causes the overactivity.
But there is no need to throw away these drugs. Other researchers warned that Maria Carilo, chief scientific officer of the Zheimer Society, an American charity for mouse experiments, said: "The mouse model is incomplete. We have been suffering from Alzheimer's disease for many years. I have been in contact with animals." The organization, Alzheimer's disease.
Busche agrees that mouse models cannot simulate all aspects of human disease.