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Neurology Neuroimmunology and Neuroinflammation

Immuno-Proteomic Features Associated to Relapse Risk in Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease

  • June 23, 2026
  • Chotima Böttcher, et al., Charité—Universitätsmedizin Berlin
Product:
CNS Disease Panel 120
Topic:
CNS
Disease Area:
MOGAD
Sample Type:
CSF
Back to Publications​
Topic/Product:
CNS Disease Panel 120
  • June 23, 2026
Disease Area:
MOGAD
Sample Type:
CSF

Abstract

Background and Objectives

Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is an inflammatory demyelinating disorder that overlaps clinically with multiple sclerosis (MS) but immunopathologically distinct. Although often considered an acute inflammatory disease, recurrent attacks in MOGAD can lead to demyelination, axonal injury, and secondary neurodegeneration. Reliable biomarkers associated with relapse risk and disease subphenotypes, including optic neuritis, remain limited. Here, we aimed to define molecular and cellular signatures that distinguish MOGAD from MS as a prototypical neuroinflammatory disease and from Alzheimer disease (AD) as a proxy of neurodegeneration and to identify candidate immune–proteomic features associated with relapse frequency and clinical phenotype in MOGAD.

Methods

CSF, serum, and whole-blood samples from patients with MOGAD (n = 67), MS (n = 49), and AD (n = 36) were profiled using NULISAseq™ CSF proteomics, Olink Explore 3072 CSF and serum proteomics, and high-dimensional mass cytometry for immune cell characterization. In MOGAD, longitudinal clinical data, including total attack counts from the earliest documented attack through follow-up, were integrated with immune and proteomic profiles to assess associations with disease course and clinical phenotype.

Results

CSF and blood proteomic profiling revealed distinct inflammatory and cardiometabolic proteomic profiles in MOGAD, differentiating it from both MS and AD. Compared with MS, MOGAD showed relative reductions in lymphocyte populations with regulatory phenotypes. Within MOGAD, relapsing disease was associated with reduced frequencies of CD8+CCR7+CD31+CTLA4+ T cells and concurrent expansion of double-negative γδ T-cell subsets. IL-13 correlated positively with relapse frequency and inversely with circulating regulatory T cells, whereas IL-32 and CASP4 showed opposite associations, correlating negatively with relapse count and positively with Treg frequency. IL-13 was also inversely associated with CD31-expressing CD8+ T cells. Phenotype-stratified analyses suggested that these immune-proteomic relationships differed according to clinical presentation, including optic neuritis vs nonoptic neuritis phenotypes.

Discussion

This integrative immune-proteomic analysis identifies cellular and molecular features associated with relapsing vs monophasic MOGAD, suggesting a model of impaired peripheral immune regulation in relapsing disease. While exploratory, these findings generate a concrete hypothesis for future longitudinal and functional studies aimed at refining biomarker-based monitoring and informing individualized therapeutic strategies in MOGAD.
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Authors & Affiliations

Gerardina Gallaccio¹˒²˒³*, Anna Müller¹˒²˒³*, Meng Wang¹˒²˒³, Lisa-Marie Diekmann¹˒²˒³, Carolin Otto⁴, Alessandro Dinoto⁵, Vanessa Chiodega⁵, Carolin Schwake⁶, Sven Jarius⁷, Tatiana Usnich⁸, Pia Sophie Sperber⁴, Lina Anderhalten⁸, Tatchaporn Ongphichetmetha⁹, Angus Byars¹⁰, Deni Subasic¹⁰, Desiree Kunkel¹¹, Ilya Ayzenberg⁶, Sara Mariotto⁵, Sara Samadzadeh¹˒²˒³†, Friedemann Paul¹˒²˒³˒⁴˒⁸†, and Chotima Böttcher¹˒²˒³†

¹ Experimental and Clinical Research Center, a cooperation between the Max Delbrück Center for Molecular Medicine in the Helmholtz Association and Charité Universitätsmedizin Berlin, Germany
² Charité—Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Germany
³ Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC), Berlin, Germany
⁴ Department of Neurology with Experimental Neurology, Charité—Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Germany
⁵ Neurology Unit, Department of Neurosciences, Biomedicine and Movement Sciences, University of Verona, Italy
⁶ Department of Neurology, St. Josef Hospital, Ruhr University Bochum, Germany
⁷ Division of Neuroimmunology, Department of Neurology, University of Heidelberg, Germany
⁸ Neuroscience Clinical Research Center, Charité—Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Germany
⁹ Siriraj Neuroimmunology Center, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, Thailand
¹⁰ F. Hoffmann-La Roche Ltd. (A.B., D.S.), Basel, Switzerland
¹¹ Flow & Mass Cytometry Core Facility, Berlin Institute of Health at Charité – Universitätsmedizin Berlin, Germany

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Steve Williams, MD, PhD

CSO

Dr. Willams serves as the company’s Chief Scientific Officer. He was previously Chief Medical Officer at Standard Biotools and at SomaLogic where he pioneered the discipline for discovery and validation of predictive, diagnostic and prognostic models using machine-learning applied to large-plex proteomics. 20 such tests were used for drug characterization, safety and efficacy when incorporated in clinical drug trials at Pharma/Biotech and 17 different multivariate tests were validated and translated into regulated healthcare uses. Prior to SomaLogic, Dr. Williams was at Pfizer in the UK and the USA as a clinical triallist in Translational Medicine, and subsequently as VP, Global Clinical Technology. He sat on the National Advisory Council for the National Institute of Biomedical Imaging and Bioengineering, the Executive Committee for the FNIH Biomarkers Consortium, and worked with FDA and PhRMA on developing evidentiary standards for biomarker qualification. Dr. William’s medical training was in London, at Charing Cross and Westminster Medical School, followed by a PhD in medicine/physiology at the same institution and training in Radiology at the University of Newcastle Upon Tyne. Steve is co-inventor on 26 proteomics patents and author/coauthor on multiple foundational proteomics manuscripts.

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Justin McAnear

CFO

Mr. McAnear serves as the company’s Chief Financial Officer. He brings over 25 years of operational and financial leadership experience across various sectors and was instrumental in taking 10x Genomics public in 2019, serving as its CFO for over five years. Mr. McAnear served for over 3 years as Tesla’s VP of Worldwide Finance and Operations, supporting landmark initiatives such as the Model X and Model 3 launches and Solar City acquisition.  He also held various roles at Apple and J&J earlier in his career and served as a naval officer and aviator for over 9 years.