Greg Duncan

Myelin is proteolipid that ensheathes the long processes of neurons (termed axons) which carry information to and from the brain. It greatly enhances the speed of conduction and reduces the energy use within the axon. Diseases like periventricular leukomalacia in infants, multiple sclerosis (MS) in adults or simply traumatic injury can damage myelin. Regeneration of myelin occurs in most MS patients, but is often incomplete. A failure to regenerate myelin is associated with increased axon loss, the main correlate of progressive disability in MS patients.
Previously, I determined that myelin regulatory factor (myrf), an essential transcription factor for myelination during development, is also required for myelin repair. Endogenous oligodendrocyte precursor cells (OPCs) normally produce new oligodendrocytes which regenerate myelin in response to damage. However, when myrf is removed from OPCs, mice are unable to generate new myelin. Demyelinated lesions in these mice mimic chronically demyelinated lesions in MS patients, where OPCs are unable to mature into new remyelinating oligodendrocytes. I am currently examining the functional and anatomical consequences of impaired remyelination in a mouse model of MS.