Oligodendrocyte Injury in Multiple Sclerosis.

Introduction: Multiple sclerosis (MS) is a chronic autoimmune disorder of the central nervous system (CNS), marked by inflammation, demyelination, and significant oligodendrocyte injury. This disease arises from a complex interplay of genetic predispositions and environmental triggers that drive immune-mediated damage to oligodendrocytes and myelin proteins. This research paper explores the multifaceted aspects of oligodendrocyte injury in MS, ranging from underlying pathophysiological mechanisms to potential therapeutic interventions and translational implications for clinical practice. Oligodendrocyte damage in MS occurs via multiple mechanisms, including metabolic stress, oxidative damage, and cytokine-induced apoptosis, mainly mediated by interferon-gamma (IFN-γ) signaling. This process exacerbates neuroinflammation and contributes to disease progression. Emerging therapeutic strategies, such as targeting metabolic pathways, reducing oxidative stress, and enhancing autophagy, have demonstrated potential in preclinical studies. Furthermore, stem cell therapies are being explored for their ability to regenerate oligodendrocytes and restore myelin integrity. Conclusions: The intricate interplay among oligodendrocyte injury, demyelination, and neuroinflammation is central to multiple sclerosis (MS) pathogenesis. Oligodendrocytes safeguard myelin in the CNS, facing challenges from immune attacks to metabolic stress. Understanding oligodendrocyte dysfunction is vital for targeted therapies that suppress immune damage and promote remyelination and CNS repair. MS's etiology,