Inhibiting TLR7, an immune signaling protein, may help preserve the protective layer surrounding nerve fibers in the brain during both Alzheimer’s disease and ordinary aging, suggests a study led by researchers at Weill Cornell Medicine. The research is published in the journal Science.
Most nerve fibers in vertebrates are encased in sheaths made largely of myelin, a protein that protects the fibers and greatly enhances the efficiency of their signal conduction. The destruction of myelin sheaths—demyelination—can occur in the context of brain inflammation and can lead to cognitive, movement and other neurological problems. The phenomenon is seen in multiple sclerosis (MS), Alzheimer’s, Parkinson’s and other neurological conditions, as well as in ordinary aging.
Demyelination-linked disorders often show sex differences, and in the study, the researchers looked for underlying mechanisms of demyelination that might help explain these differences. Their experiments in mouse models of Alzheimer’s uncovered TLR7 as a driver of inflammatory demyelination especially in males, but also showed that removing or inhibiting this immune protein can protect against demyelination in both males and females.
