阿尔茨海默病 z-bo 2020-11-06 373

　　Can it also make Alzheimer's disease worse? Animal studies similar to the treatment of Alzheimer’s in humans have shown that the treated antibodies may actually be harmful.

　　It has been discovered that antibodies that are undergoing human trials can destroy the sticky plaques that form in the brain. In the mouse model of Alzheimer's disease, the antibodies seem to make brain cells more active in the same way and eventually stop functioning.

　　"We think this may be the failure mechanism of these antibodies in human trials." said Marc Busche of the Technical University of Munich, Germany.

　　Busche and his colleagues gave Alzheimer's disease model mice and normal mice the same antibody drug. After treatment, they found that the diseased mice had brain cells 5 times more active than normal mice.

　　plaque rupture

　　When plaques in Alzheimer's disease form, fragments of β-amyloid protein gather together. Busche and colleagues previously discovered that β-amyloid can cause neuronal hyperactivity. They believe that when antibodies destroy these plaques, it exacerbates this effect to some extent than when the plaques remain intact.

　　In the process of trying to treat Alzheimer's disease, after multiple failures, drug developers began to try to detect and treat the disease earlier.

　　Therefore, Busche and his team even studied the effects of drugs in the early stages of Alzheimer's disease in these mice. At this time, there were no plaques in their brains, neurons became more active, and symptoms of disease worsened.

　　mice may be misleading us

　　"We found that even very young mice became active before plaques were deposited, Busche said. It is unclear what causes hyperactivity.

　　However, there is no need to throw away these medicines yet. Other researchers are careful to say that mouse experiments have a history of misleading results. "The mouse model is imperfect-we have been exposed to animal Alzheimer's disease for many years," said Maria Carrillo, chief scientific officer of the American Charity Alzheimer's Association.

　　Busche agrees that mouse models cannot simulate all aspects of human disease. He said: "Targeted treatment of beta amyloid symptoms is still promising, but in the end we may need a combination of multiple methods."