Kyoto: The loss of a specific immune-regulating protein in the brain could lead to reduced levels of amyloid beta, a key factor in Alzheimer's disease, and enhance cognitive function, according to a group of researchers including those from Kyoto University.
According to Philippines News Agency, the research team discovered that the TIM-3 protein, found in microglia, which are a type of immune cell in the brain, increases as the brain ages. By genetically modifying mice with Alzheimer's disease to remove this protein, the researchers observed a 50 to 60 percent reduction in amyloid beta accumulation, along with an improvement in the mice's cognitive abilities.
Published in the journal Nature, this study holds promise for developing new treatments for Alzheimer's disease. While drugs like lecanemab, which eliminate amyloid beta, have garnered attention recently, they carry potential side effects such as brain swelling and bleeding. The research group suggests that a drug targeting TIM-3 might be used alongside lecanemab to mitigate these risks.
Kimitoshi Kimura, a lecturer at Kyoto University, noted the potential of other substances in microglia to remove amyloid beta and expressed a desire to utilize them in treating neurological diseases, including Alzheimer's.