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Review
. 2023 Dec 7:14:1216477.
doi: 10.3389/fneur.2023.1216477. eCollection 2023.

Delimiting MOGAD as a disease entity using translational imaging

Frederike Cosima Oertel #  1   2   3 , Maria Hastermann #  1   2 , Friedemann Paul  1   2   3
Affiliations
Review

Delimiting MOGAD as a disease entity using translational imaging

Frederike Cosima Oertel et al. Front Neurol. .

Erratum in

Abstract

The first formal consensus diagnostic criteria for myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) were recently proposed. Yet, the distinction of MOGAD-defining characteristics from characteristics of its important differential diagnoses such as multiple sclerosis (MS) and aquaporin-4 antibody seropositive neuromyelitis optica spectrum disorder (NMOSD) is still obstructed. In preclinical research, MOG antibody-based animal models were used for decades to derive knowledge about MS. In clinical research, people with MOGAD have been combined into cohorts with other diagnoses. Thus, it remains unclear to which extent the generated knowledge is specifically applicable to MOGAD. Translational research can contribute to identifying MOGAD characteristic features by establishing imaging methods and outcome parameters on proven pathophysiological grounds. This article reviews suitable animal models for translational MOGAD research and the current state and prospect of translational imaging in MOGAD.

Keywords: EAE; animal models; imaging; myelin oligodendrocyte glycoprotein associated disease; translational research.

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Conflict of interest statement

FP reports research support from Bayer, Novartis, Biogen, Teva, Sanofi-Aventis/Genzyme, Alexion, Roche and Merck Serono and 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, Guthy-Jackson Charitable Foundation, and NMSS. He also reports receiving consultation fees as an associate editor for Neurology, Neuroimmunology, and Neuroinflammation and as an academic editor for PLoS ONE and consultant fees for Sanofi Genzyme, Biogen, MedImmune, Shire, and Alexion. He also reports receiving speaker honoraria from Bayer, Novartis, Biogen, Teva, Sanofi-Aventis/Genzyme, Merck Serono, Alexion, Chugai, MedImmune, and Shire. He is an advisory board member for Novartis and MedImmune Scientific and holds stocks of Nocturne GmbH—all outside the submitted work. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
MR imaging of the spinal cord in people with MOGAD. Sagittal T2-weighted MRI showing hyperintense lesions in line with (A) an LETM and (B) shorter lesions. Axial T2-weighted MRI showing (C) a centrally located lesion and (D) the characteristic H-sign. LETM, longitudinally extensive transverse myelitis; MOGAD, myelin oligodendrocyte glycoprotein antibody associated disease; MRI, magnetic resonance imaging.
Figure 2
Figure 2
Clinical imaging of retina and optic nerve. T2-weighted MRI of the optic nerve (A) showing a longitudinal lesion with edema. OCT quantifying retinal neuroaxonal content measured by pRNFL around the optic nerve head in a retina without a history of ON (B) and with a history of ON (C) in MOGAD: scanning laser ophthalmoscopy (B.1, C.1), color-coded comparison with a healthy control cohort (B.2, C.2) and cross-sectional B-scans showing pRNFL atrophy in (C.3) compared with (B.3). MOGAD, myelin oligodendrocyte glycoprotein antibody associated disease; MRI, magnetic resonance imaging; OCT, optical coherence tomography; ON, optic neuritis; pRNFL, peripapillary retinal nerve fiber layer.
See this image and copyright information in PMC

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