Deciphering the missing links between Friedreich ataxia and multiple sclerosis for targeted drug development

Abstract

Neurodegenerative diseases (NDDs), such as Friedreich ataxia (FA) and multiple sclerosis (MS), are marked by progressive neurodegeneration and heterogeneous pathologies. Despite distinct aetiologies, FA and MS appear to share some overlapping molecular mechanisms, including iron and lipid dysregulation, mitochondrial dysfunction, oxidative stress, and neuroinflammation. Recent research, including comparative transcriptomic analyses, offers valuable insights into shared disease pathways, with implications for potential biomarkers and therapeutic targets. In this review, we explore the shared pathological features and disease mechanisms in FA and MS, highlighting how delineating these shared pathways could inform early diagnostic strategies and support the development of targeted, mechanism-based interventions, including opportunities for drug repurposing.