The results of newly reported preclinical research indicate that a genetic mutation that helps animals including yaks and Tibetan antelopes survive at high altitudes may hold the key to repairing nerve damage in demyelinating disorders such as cerebral paralysis and multiple sclerosis (MS). The study headed by Liang Zhang, PhD, at Songjiang Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, identified a naturally existing pathway which studies in multiple myelin injury models in mice showed could be stimulated to promote nerve remyelination. The researchers suggest their findings could point to new strategies for treating diseases including MS using the body’s own repair pathways. Zhang is senior and corresponding author of the team’s published paper in Neuron, titled “A gain-of-function Retsat variant from high-altitude adaptation promotes myelination via a neuronal dihydroretinoic acid-RXR-γ pathway,” in which the investigators wrote, “This study begins with a genetic variant associated with high altitude adaptation and uncovers a core regulatory axis for CNS myelination and repair.” The myelin sheath is a protective layer, produced by cells called oligodendrocytes, that surrounds nerve fibers in the brain and spinal cord, allowing nerve signals to transmit efficiently. This myelin sheath is produced by oligodendrocytes. Insufficient oxygen during brain development can damage this layer, leading to conditions such as cerebral paralysis in newborns. In adults, injuries to the myelin sheath are linked with MS, an autoimmune disease in which the immune system mistakenly attacks and destroys the myelin sheath. Reduced blood flow to the brain, often associated with aging, can also damage myelin, contributing to conditions such as cerebral small vessel disease and vascular dementia. In…
