Agglutinated proteins in the brain, known as amyloid-β plaques, are a key characteristic of Alzheimer’s. One treatment option uses special antibodies to break down these plaques.
This approach yielded good results in the animal model, but for reasons that are not yet clear, it has so far been unsuccessful in patient studies.
Scientists at the Technical University of Munich (TUM) have now discovered one possible cause: they noticed that, in mice that received one antibody treatment, nerve cell disorders did not improve and were even exacerbated.
This article originally appeared on Psychiatry Advisor
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