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 the group removed the protein from a mouse with Alzheimer's disease by genetic modification, the accumulation of amyloid beta decreased by 50% to 60%, 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.
"There may be other substances in microglia that can be used to remove causes such as amyloid beta," said Kimitoshi Kimura, a lecturer at Kyoto University. "We want to use them to treat neurological diseases, including Alzheimer's."
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