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Abstract #0058

A quantification of myelin and axonal damage across multiple sclerosis lesions and clinical subtypes with myelin and diffusion MRI

Reza Rahmanzadeh1,2, Po-Jui Lu1,2, Muhamed Barakovic1,2, Riccardo Galbusera1,2, Matthias Weigel1,2,3, Pietro Maggi4, Thanh D. Nguyen 5, Simona Schiavi6, Francesco La Rosa 7,8, Daniel S. Reich9, Pascal Sati9, Yi Wang5, Meritxell Bach-Cuadra7,8, Ernst-Wilhelm Radue1, Jens Kuhle2, Ludwig Kappos2, and Cristina Granziera1,2
1Translational Imaging in Neurology (ThINk) Basel, Department of Medicine and Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland, 2Neurologic Clinic and Policlinic, Departments of Medicine, Clinical Research and Biomedical Engineering, University Hospital Basel and University of Basel, Basel, Switzerland, 3Radiological Physics, Department of Radiology, University Hospital Basel, Basel, Switzerland, 4Department of Neurology, Lausanne University Hospital, Lausanne, Switzerland, 5Department of Radiology, Weill Cornell Medical College, New York, NY, United States, 6Department of Computer Science, University of Verona, Verona, Italy, 7Signal Processing Laboratory (LTSS), Ecole polytechnique fédérale de Lausanne (EPFL), Lausanne, Switzerland, 8Radiology Department, Center for Biomedical Imaging, Lausanne University and University Hospital, Lausanne, Switzerland, 9National Institute of Neurological Disorders and Stroke, Translational Neuroradiology Section, Division of Neuroimmunology and Neurovirology, Bethesda, MD, United States

The interplay between axonal and myelin damage in multiple sclerosis (MS) is poorly understood. This study aimed to evaluate the concomitant presence of axonal and myelin injury in living MS patients by using myelin and multi-shell diffusion MRI. Confirming neuropathological findings, our results show that (i) axonal and myelin damage exists in MS lesions and spreads out from the lesions in a centrifugal way, (ii) the extent of myelin and axonal damage differs among lesion subtypes and according to lesion anatomical locations and (iii) axonal (and not myelin) damage differs between relapsing-remitting and progressive MS patients.

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