MYELIN-OLIGODENDROCYTE-GLYCOPROTEIN (MOG) AUTOANTIBODIES AS POTENTIAL MARKERS OF SEVERE OPTIC NEURITIS AND SUBCLINICAL RETINAL AXONAL DEGENERATION

Introduction: Neuromyelitis optica spectrum disorder (NMOSD), recurrent optic neuritis (rON), multiple sclerosis (MS), and anti-NMDAR encephalitis are neurological conditions that can lead to severe optic neuritis and retinal axonal degeneration. Myelin-oligodendrocyte-glycoprotein autoantibodies (MOG-abs) have been identified in subgroups of these disorders, suggesting a role in disease pathology. This study explores whether MOG-abs can serve as markers for retinal axonal degeneration using optical coherence tomography (OCT) in a diverse cohort of patients.

Key Findings: The study evaluated 13 MOG-abs-positive patients, including those with rON, adult MS, relapsing encephalomyelitis, and aquaporin-4-abs (AQP4-abs)-negative NMOSD. Controls included 13 MOG-abs and AQP4-abs-negative MS patients matched by age, sex, and ON episodes and 13 healthy controls (HC). Additionally, 19 unmatched AQP4-abs-positive MOG-abs-negative NMOSD subjects were investigated. The results showed that global peripapillary retinal nerve fiber layer (pRNFL) thickness was significantly reduced in MOG-abs-positive patients compared to MOG-abs-negative MS, HC, and AQP4-abs-positive NMOSD subjects. Non-ON eyes from MOG-abs-positive subjects exhibited significant subclinical atrophy in the temporal pRNFL quadrants. Moreover, microcystic macular edema (MME) was observed in MOG-abs-positive patients and AQP4-abs-positive NMOSD subjects but not in MOG-abs-negative MS or HC.

Innovative Tools: The researchers utilized OCT to assess retinal nerve fiber layer thickness and detect subclinical axonal degeneration. This non-invasive imaging technique provided detailed measurements of pRNFL and macular regions, allowing for the identification of retinal abnormalities associated with MOG-abs. The study also included using MOG-abs and AQP4-abs assays to classify patients accurately.

Behavioral Assessments: The study did not include behavioral assessments as it focused on the anatomical and pathological changes in the retina associated with MOG-abs. However, the clinical implications of retinal degeneration and the presence of MME can significantly impact visual function and quality of life in patients with NMOSD, MS, and related disorders.

Biochemical Analysis: The presence of MOG-abs was determined using specific assays, and the relationship between these autoantibodies and retinal degeneration was explored. The study highlighted that MOG-abs-related OCT features are predominant in the temporal pRNFL quadrants, resembling the retinal pattern seen in MS but potentially more severe than in AQP4-abs-positive NMOSD. This suggests a distinct pathological mechanism involving MOG-abs in retinal degeneration.

Conclusions: MOG-abs are significantly associated with severe optic neuritis and retinal axonal degeneration, making them potential markers for these conditions. The study's findings indicate that MOG-abs-related OCT features, particularly in the temporal pRNFL quadrants, can indicate subclinical pathology and may be linked to MME. These insights could enhance diagnosing and monitoring patients with NMOSD, rON, MS, and related disorders, guiding more targeted therapeutic interventions. Future research should further explore the long-term impact of MOG-abs on retinal health and the potential benefits of early detection and treatment.

Join the Discussion: We invite you to share your thoughts on the role of MOG-abs in retinal axonal degeneration and their potential as diagnostic markers. How might these findings influence the management and treatment of patients with NMOSD, MS, and related conditions? What other biomarkers could complement the use of MOG-abs in clinical practice? Join the conversation in the comments below and share your insights and ideas.

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Original Research: The original research, "Myelin-oligodendrocyte-glycoprotein (MOG) autoantibodies as potential markers of severe optic neuritis and subclinical retinal axonal degeneration," is available on PubMed here.