IMAGINE-NeMOG: Imaging Antibody-Mediated CNS Disorders: Conventional and Advanced MRI in NMOSD and MOGAD


The IMAGINE-NeMOG research line focuses on the comprehensive characterization of neuromyelitis optica spectrum disorder (NMOSD) and myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) through the integration of conventional and advanced MRI techniques. Although these antibody-mediated inflammatory disorders are defined by acute attacks targeting the optic nerves, spinal cord, and brain, the structural substrates of tissue injury, mechanisms of recovery, and long-term disability remain insufficiently understood.

We combine clinical MRI sequences with quantitative approaches - including volumetric analysis, diffusion and myelin-sensitive imaging, spinal cord morphometry, and other advanced metrics - to investigate both lesion-related and non-lesional tissue alterations. Multimodal imaging data are systematically integrated with detailed clinical phenotyping, antibody status, and longitudinal follow-up, enabling a refined characterization of disease-specific patterns of damage.

A core component of this research line is the application of computational modelling and artificial intelligence methods to multimodal imaging datasets. Machine learning and data-driven approaches are used to identify imaging signatures that differentiate NMOSD and MOGAD from multiple sclerosis to model disease trajectories, and to develop quantitative biomarkers that may support patient stratification and mechanism-informed clinical decision-making.

By linking imaging-derived metrics to biological processes and clinical outcomes, IMAGINE-NeMOG aims to advance a more precise and quantitative framework for antibody-mediated inflammatory CNS disorders, in line with a translational and modelling-oriented approach to neuroimaging.


Examples of lesion in a patient with MOGAD

lesion in a patient with MOGAD

Example of a lesion in a patient with MOGAD that completely resolves on FLAIR imaging over 5 months, accompanied by a corresponding shift in QSM signal from hyperintense to isointense.


other example

Example of a persistent temporal cortical lesion and an infratentorial lesion in a patient with MOGAD, following the resolution of most other lesions, demonstrated using a multiparametric approach with advanced myelin-sensitive imaging techniques.

Rosa Cortese

Rosa Cortese

Rosa Cortese, MD, PhD is a neurologist and neuroscientist specializing in neuroimmunology and advanced neuroimaging. She is currently a Senior Researcher at the Research Center for Clinical Neuroimmunology and Neuroscience (RC2NB), University Hospital Basel.

She completed her PhD in Neurology at University College London (UCL) and subsequently worked as a Lecturer in Neurology at the University of Siena, developing a strong track record in international research collaborations.

Her research focuses on imaging biomarkers and disease mechanisms in multiple sclerosis (MS), myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD), and AQP4-positive neuromyelitis optica spectrum disorders (NMOSD). She is particularly interested in brain and spinal cord lesions and atrophy, disease progression, and the application of advanced MRI and deep learning models to improve diagnosis and prognosis.

Dr. Cortese is an active member of international networks including MAGNIMS (Magnetic Resonance Imaging in Multiple Sclerosis) and MEDEN (MOGAD Eugène Devic European Network), contributing to large multicenter studies aimed at improving the understanding and differentiation of demyelinating diseases.

1. Cortese R, Sforazzini F, Gentile G, et al. Deep learning modeling to differentiate multiple sclerosis from MOG antibody-associated disease. Neurology. 2025;105(6):e214075.

2. Cortese R, Battaglini M, Prados F, et al.; MAGNIMS Study Group. Grey matter atrophy and its relationship with white matter lesions in MOGAD, AQP4-NMOSD, and multiple sclerosis. Ann Neurol. 2024;96(2):276–288.

3. Geraldes R, Arrambide G, Banwell B, et al.; MAGNIMS Study Group. The influence of MOGAD on the diagnosis of multiple sclerosis using MRI. Nat Rev Neurol. 2024;20(10):620–635.

4. Cortese R, Battaglini M, Prados F, et al.; MAGNIMS Study Group. Clinical and MRI measures to identify non-acute MOG antibody disease in adults. Brain. 2023;146(6):2489–2501.

5. Cortese R, Prados F, Tur C, et al. Differentiating multiple sclerosis from AQP4-NMOSD and MOG antibody disease with imaging. Neurology. 2023;100(3):e308–e323.

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