MIT study identifies key pathway by which Alzheimer's risk gene APOE4 disrupts neuron insulation
Researchers restore myelination by targeting molecular mechanism in lab experiments
A new study from the Picower Institute for Learning and Memory at MIT has uncovered one of the main mechanisms by which the APOE4 gene variant, the biggest genetic risk factor for late-onset Alzheimer's disease, impairs brain circuit function. The research, published Oct. 15 in Cell Stem Cell, shows that APOE4 suppresses Wnt signaling in oligodendrocytes, the cells that insulate neurons with a fatty sheath called myelin. This disrupts myelination and causes lipid droplets to accumulate in the cells. By restoring Wnt signaling, the team was able to reverse the damage in both human cell cultures and in mice.