Restoring DSCAM expression mitigates neuronal morphology and axon guidance deficits in Down syndrome

This study demonstrates that DSCAM overexpression—resulting from chromosome 21 triplication in Down syndrome—impairs neuronal development and axon guidance in both mouse models and human-derived neurons. Remarkably, normalizing DSCAM levels rescues these neuronal developmental deficits, suggesting a potential therapeutic approach for addressing some neurobiological features of Down syndrome.