Serum glial fibrillary acidic protein correlates with retinal structural damage in aquaporin-4 antibody positive neuromyelitis optica spectrum disorder
Authors
- T.Y. Lin
- P. Schindler
- U. Grittner
- F.C. Oertel
- A. Lu
- S. Motamedi
- S.K. Yadav
- A.S. Duchow
- S. Jarius
- J. Kuhle
- P. Benkert
- A.U. Brandt
- J. Bellmann-Strobl
- T. Schmitz-Hübsch
- F. Paul
- K. Ruprecht
- H.G. Zimmermann
Journal
- Multiple Sclerosis and Related Disorders
Citation
- Mult Scler Relat Disord 67: 104100
Abstract
BACKGROUND: Aquaporin-4 immunoglobulin-G positive (AQP4-IgG+) neuromyelitis optica spectrum disorder (NMOSD) is an autoimmune astrocytopathy associated with optic neuritis (ON). Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is an oligodendrocytopathy with similar phenotype. Serum glial fibrillary acidic protein (sGFAP), an astrocyte-derived protein, is associated with disease severity in AQP4-IgG+ NMOSD. Serum neurofilament light (sNfL) indicates neuroaxonal damage. The objective was to investigate the association of sGFAP and sNfL with subclinical afferent visual system damage in clinically stable AQP4-IgG+ NMOSD and MOGAD patients. METHODS: In this cross-sectional study, clinically stable patients with AQP4-IgG+ NMOSD (N=33) and MOGAD (N=16), as diseased controls, underwent sGFAP and sNfL measurements by single molecule array, retinal optical coherence tomography and visually evoked potentials. RESULTS: Higher sGFAP concentrations were associated with thinner ganglion cell-inner plexiform layer (ß(95% confidence interval (CI)) = -0.75(-1.23 to -0.27), p=0.007) and shallower fovea (average pit depth: ß(95%CI) = -0.59(-0.63 to -0.55), p=0.020) in NMOSD non-ON eyes. Participants with pathological P100 latency had higher sGFAP (median [interquartile range]: 131.32 [81.10–179.34] vs. 89.50 [53.46–121.91]pg/ml, p=0.024). In MOGAD, sGFAP was not associated with retinal structural or visual functional measures. CONCLUSIONS: The association of sGFAP with structural and functional markers of afferent visual system damage in absence of ON suggests that sGFAP may be a sensitive biomarker for chronic disease severity in clinically stable AQP4-IgG+ NMOSD.