Reducing the methylation of a key messenger RNA can promote migration of macrophages into the brain and ameliorate symptoms of Alzheimer’s disease in a mouse model, according to a new study publishing March 7 in the open access journal PLOS Biology by Rui Zhang of Air Force Medical University in Xian, Shaanxi, China. The results illuminate one pathway for entrance of peripheral immune cells into the brain, and may provide a new target for treatment of Alzheimer’s disease.
A presumed trigger for the development of Alzheimer’s disease is the accumulation of proteinaceous, extracellular amyloid-beta plaques in the brain. High levels of amyloid-beta in mice leads to neurodegeneration and cognitive symptoms reminiscent of human Alzheimer’s disease, and reduction of amyloid-beta is a major goal in development of new treatments.
One potential pathway for getting rid of amyloid-beta is the migration of blood-derived myeloid cells into the brain, and their maturation into macrophages, which, along with resident microglia, can consume amyloid-beta. That migration is a complex phenomenon controlled by multiple interacting players, but a potentially important one is the methylation of messenger RNA within the myeloid cells.
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