Loss of Immune-Regulating Protein Eases Alzheimer's Disease

Loss of Immune-Regulating Protein Eases Alzheimer's Disease

   Tokyo, May 8 (Jiji Press)--The loss of a certain immune-regulating protein in the brain leads to a decrease in the levels of amyloid beta, which causes Alzheimer's disease, and improves cognitive function, a group of researchers including from Kyoto University has found.
   The group confirmed that the TIM-3 protein, which exists in microglia, a type of immune cell in the brain, increases as the brain ages. When it removed the protein from a mouse with Alzheimer's disease by genetic modification, the accumulation of amyloid beta decreased by 50 to 60 pct, and the mouse showed an improvement in cognitive function.
   The study, published in the journal Nature, is expected to help develop a new treatment for the disease.
   In recent years, lecanemab, a drug that removes amyloid beta, has attracted attention. However, there are concerns about its side effects, such as brain swelling and bleeding.
   A possible drug based on TIM-3 could be used with lecanemab to reduce the risk of side effects, the research group said.

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