Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease (MOGAD): Mechanisms, Syndromes, and Management

Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) has emerged as a distinct demyelinating condition with unique clinical and radiographic characteristics that differentiate it from multiple sclerosis (MS) and aquaporin-4 antibody-positive neuromyelitis optica spectrum disorder (AQP4-NMOSD). This review provides a clinically focused update tailored for ophthalmologists, emphasizing the ocular manifestations, diagnostic workup, and current treatment strategies for MOGAD. Optic neuritis is the most common presenting symptom in MOGAD. It can frequently manifest as bilateral involvement or severe optic disc edema and often has a more favorable prognosis for visual recovery compared with AQP4-NMOSD. Recent advances in neuroimaging, optical coherence tomography (OCT), and the development of live cell-based antibody assays have significantly enhanced diagnostic accuracy and characterization of the disease. Differentiating features such as the absence of classic MS lesions on MRI, longitudinally extensive optic nerve involvement, and specific cerebrospinal fluid findings are essential for guiding diagnosis. Treatment strategies continue to evolve for MOGAD. High-dose corticosteroids remain the mainstay of acute management, whereas long-term immunotherapy, that is, intravenous immunoglobulin (IVIg), rituximab, and other steroid-sparing agents, has shown efficacy in reducing relapse risk. Optimal maintenance regimens are still under investigation, and treatment must be individualized based on relapse risk, availability, and tolerability. Rapid recognition and accurate diagnosis are critical for preventing permanent vision loss and neurological disability. This article aims to provide ophthalmologists with a practical reference for identifying, evaluating, and managing MOGAD, distinguishing it from other optic neuropathies, and implementing evidence-based treatment to improve patient outcomes.