
Researchers have found that blocking the PD-L1 protein restores microglial function and reduces neuronal hyperactivity in a mouse model of Alzheimer's disease, opening new prospects for therapy.
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In Alzheimer's disease, microglia are disrupted and neurons become overactive.
Scientists have found a way to restore the functioning of immune cells in the brain and reduce excessive neuronal activity in Alzheimer's disease. The new approach was successfully tested on mice. The study was published in the journal Science Advances.
In Alzheimer's disease, the work of microglia, the brain's immune cells that respond to damage and help maintain the normal state of nervous tissue, is disrupted. At the same time, neurons may become overactive, which is also considered a sign of brain dysfunction.
Scientists have discovered that these processes are influenced by the immune proteins PD-1 and PD-L1. Researchers blocked PD-L1 in a mouse model of Alzheimer's disease using a special antibody.
After injecting the drug directly into the brain, microglia again began to respond more actively to damaged areas, and the abnormally high activity of neurons decreased. This indicates a partial restoration of impaired brain functions, but scientists have not tested whether this approach slows down the development of the disease itself and memory deterioration.
According to the authors, controlling immune processes in the brain could become a new direction in the treatment of Alzheimer's disease.

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