Targeting brain protein may offer new hope for Alzheimer’s treatment

A team of researchers, including scientists from Kyoto University, has discovered that eliminating a specific immune-regulating protein in the brain significantly reduces levels of amyloid beta, the substance linked to Alzheimer’s disease, and enhances cognitive performance.

Their findings, recently published in the journal Nature, focus on TIM-3, a protein found in microglia, the brain’s resident immune cells. The study showed that TIM-3 levels increase as the brain ages.

By genetically removing TIM-3 in mice engineered to develop Alzheimer’s, researchers observed a 50–60% reduction in amyloid beta buildup and notable improvements in the animals’ cognitive abilities.

This discovery could pave the way for new treatment strategies targeting the root cause of Alzheimer’s. Current therapies, such as lecanemab, which works by clearing amyloid beta, have shown promise but also raise safety concerns, including risks of brain swelling and bleeding.

The researchers believe that a therapy targeting TIM-3 could potentially be used alongside lecanemab to reduce these side effects. They also see promise in exploring other substances within microglia that may contribute to eliminating harmful proteins from the brain.

“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.”