“The Interaction Between Oxidative Stress and Neurosteroid Imbalance in Multiple Sclerosis: Exploring a New Pathway in Disease Mechanisms and Potential Treatment Approaches”

Multiple sclerosis (MS) is a chronic autoimmune disorder of the central nervous system (CNS) characterized by damage and destruction of neurons. Although its precise cause remains unclear, growing evidence points to oxidative stress as a key contributor to MS onset and progression. Excessive production of reactive nitrogen species (RNS) and reactive oxygen species (ROS) can impair cellular components, accelerating demyelination and axonal loss. This process involves both the central and peripheral nervous systems, with various cells such as microglia, astrocytes, and T cells playing significant roles in mediating the damage. In contrast, neurosteroids—steroids synthesized within the CNS—have gained attention for their neuroprotective and anti‐inflammatory properties. These compounds regulate neural excitability, synaptic function, and immune responses. Disruptions in the production or function of neurosteroids may contribute to the pathogenesis of neurological disorders, including MS. Although both oxidative stress and neurosteroid dysregulation have been individually implicated in MS pathology, their interplay remains poorly understood. Investigating how these two pathways interact could provide deeper insights into MS mechanisms and highlight novel therapeutic avenues aimed at restoring neurosteroid balance to reduce disease‐related damage.