1. Serum glial fibrillary acidic protein correlates with retinal structural damage in aquaporin-4 antibody positive neuromyelitis optica spectrum disorder.
- Author
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Lin TY, Schindler P, Grittner U, Oertel FC, Lu A, Motamedi S, Yadav SK, Duchow AS, Jarius S, Kuhle J, Benkert P, Brandt AU, Bellmann-Strobl J, Schmitz-Hübsch T, Paul F, Ruprecht K, and Zimmermann HG
- Subjects
- Humans, Glial Fibrillary Acidic Protein metabolism, Intermediate Filaments metabolism, Cross-Sectional Studies, Aquaporin 4, Autoantibodies, Immunoglobulin G, Biomarkers, Neuromyelitis Optica, Optic Neuritis diagnostic imaging, Retinal Diseases
- 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 a 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 (β (95% confidence interval (CI)) = -0.75 (-1.23 to -0.27), p = 0.007) and shallower fovea (average pit depth: β (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., Competing Interests: Declaration of Competing Interest T.-Y. Lin, P. Schindler, U. Grittner, A. Lu, A.S. Duchow, S. Jarius, J. Kuhle, P. Benkert and T. Schmitz-Hübsch report no relevant disclosures. F.C. Oertel was an employee of Nocturne GmbH and receives research support by the American Academy of Neurology, the National Multiple Sclerosis Society and Deutsche Gesellschaft für Neurologie (German Neurology Society), unrelated to this work. S. Motamedi is named as co-inventor on the patent application for the foveal shape analysis method used by this manuscript (“Method for estimating shape parameters of the fovea by optical coherence tomography”, International Publication Number: “WO 2019/016319 A1”). S.K. Yadav is named as co-inventor on the patent application for the foveal shape analysis method used by this manuscript (“Method for estimating shape parameters of the fovea by optical coherence tomography”, International Publication Number: “WO 2019/016319 A1”) and a cofounder of medical technology companies Nocturne GmbH. A.U. Brandt is cofounder and shareholder of medical technology companies Nocturne GmbH and Motognosis GmbH. He is named as inventor on several patent applications describing MS biomarkers, visual perceptive computing based motor function analysis, and retinal image analysis. J. Bellmann-Strobl has received speaking honoraria and travel grants from Bayer Healthcare, and sanofi-aventis/Genzyme, in addition received compensation for serving on a scientific advisory board of Roche, unrelated to the presented work. F. Paul served on the scientific advisory boards of Novartis and MedImmune; received travel funding and/or speaker honoraria from Bayer, Novartis, Biogen, Teva, Sanofi-Aventis/Genzyme, Merck Serono, Alexion, Chugai, MedImmune, and Shire; is an associate editor of Neurology: Neuroimmunology & Neuroinflammation; is an academic editor of PLoS ONE; consulted for Sanofi Genzyme, Biogen, MedImmune, Shire, and Alexion; received research support from Bayer, Novartis, Biogen, Teva, Sanofi-Aventis/Geynzme, Alexion, and Merck Serono; and received research support from the German Research Council, Werth Stiftung of the City of Cologne, German Ministry of Education and Research, Arthur Arnstein Stiftung Berlin, EU FP7 Framework Program, Arthur Arnstein Foundation Berlin, Guthy-Jackson Charitable Foundation, and NMSS. K. Ruprecht received research support from Novartis, Merck Serono, German Ministry of Education and Research, European Union (821283-2), Stiftung Charité (BIH Clinical Fellow Program) and Arthur Arnstein Foundation; received travel grants from Guthy-Jackson Charitable Foundation. H.G. Zimmermann received research grants from Novartis and speaking honoraria from Bayer Healthcare and Novartis., (Copyright © 2022. Published by Elsevier B.V.)- Published
- 2022
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