Genetics

Recent advances in functional genomics are reshaping our understanding of multiple sclerosis (MS) by revealing that genetic risk variants act beyond immune cells to directly influence central nervous system–resident populations. This blog post explores new evidence demonstrating that non-coding MS-associated variants exert cell-type–specific regulatory effects in oligodendroglial lineage cells, modulating key processes such as oligodendrocyte precursor cell proliferation, differentiation, and cytokine-mediated immune cell recruitment. By integrating chromatin accessibility profiling, massively parallel reporter assays, and CRISPR-based single-cell perturbation screens, the study positions oligodendroglia as active drivers—rather than passive victims—of MS pathogenesis, with important implications for disease mechanisms and therapeutic strategies