Olig2‐specific loss‐of‐function <i>Slc35a2</i> results in hypomyelination and spontaneous seizures

Our results demonstrate that loss of SLC35A2 function in oligodendrocytes is sufficient to reproduce pathological and clinical features observed in human mild malformation of cortical development with oligodendroglial hyperplasia and epilepsy. Spontaneous seizures in the absence of direct neuronal genetic abnormalities highlight a central role for oligodendrocyte dysfunction and hypomyelination in epileptogenesis. These findings challenge the neuron-centric view of epilepsy and suggest that targeting glial dysfunction may offer novel therapeutic opportunities. Further studies are warranted to delineate cellular interactions driving epileptogenesis and to explore glia-centered treatment strategies for drug-resistant epilepsies.