MIND

Multiple sclerosis (MS) and leukodystrophies are myelin disorders of the central nervous system, respectively acquired and genetically inherited diseases.

Our team investigates the neuroinflammatory and metabolic mechanisms involved in these demyelinating disorders. We focus particularly on how immune cells and cellular metabolism contribute to lesion progression and repair processes within the central nervous system.

Our research relies on integrated approaches combining high-resolution multimodal neuroimaging, humanized mouse models, functional analyses of patient-derived macrophages, and innovative theoretical models. These complementary strategies enable us to identify new therapeutic targets and develop approaches promoting neuroprotection and remyelination in MS and inflammatory leukodystrophies.

Research axis 1 – Neuroinflammation and remyelination in MS

We investigate how innate and adaptive immune cells contribute to myelin destruction and repair in multiple sclerosis, with the aim of identifying the mechanisms associated with successful remyelination or the development of chronic inflammatory lesions.

Research axis 2 – Inflammatory leukodystrophies and innovative therapies

We develop imaging biomarkers and evaluate novel therapeutic strategies targeting metabolism and inflammation in inflammatory leukodystrophies, including adrenoleukodystrophy, CSF1R-related leukodystrophy, and metachromatic leukodystrophy.

Research axis 3 – Immune metabolism and macrophage reprogramming

We study the metabolic mechanisms controlling macrophage activation in both MS and leukodystrophies in order to identify new therapeutic targets promoting neuroprotective and regenerative functions.

Main publications

• Yska HAF, Golse M, Beerepoot S, Hayer S, Bergner C, de Paiva ARB, Marelli C, Palacios NJ, Osorio YL, Huiban C, Franke G, Wortmann F, Holtick U, Ayrignac X, van der Knaap MS, Schöls L, Perlbarg V, Galanaud D, de Witte MA, Wolf NI, Nguyen S, Mochel F on behalf of the International CSF1R‐RD Working Group. Hematopoietic Stem Cell Transplantation in an International Cohort of Colony Stimulating Factor-1 Receptor (CSF1R)-Related Disorder. Mov Disord. 2025 Sep;40(9):1826-1835.
• Benamar M, Contini P, Schmitz-Abe K, Lanzetta O, Getachew F, Bachelin C, Leyva Castillo JM, Wang M, Oktelik FB, Perrot O, Batamack Y, Arbag SN, Stephen-Victor E, Harb H, Agrawal PB, Louapre C, Ivaldi F, Uccelli A, Inglese M, Angelini C, Zujovic V, De Palma R, Chatila TA. Notch3 destabilizes regulatory T cells to drive autoimmune neuroinflammation in multiple sclerosis. Immunity. 2025 Nov 11 ;58(11) :2753–2768.e6.
• Golse M, Weinhofer I, Blanco B, Barbier M, Yazbeck E, Huiban C, Chaumette B, Pichon B, Fatemi A, Pascual S, Martinell M, Berger J, Perlbarg V, Galanaud D, Mochel F. Leriglitazone halts disease progression in adult patients with early cerebral adrenoleukodystrophy. Brain. 2024 Oct 3;147(10):3344-3351.
• Girka F, Gloaguen A, Le Brusquet L, Zujovic V, Tenenhaus A. Tensor generalized canonical correlation analysis. Information Fusion. 2024; 102:102045.
• Fransson J, Bachelin C, Ichou F, Guillot-Noël L, Ponnaiah M, Gloaguen A, Maillart E, Stankoff B, Tenenhaus A, Fontaine B, Mochel F, Louapre C, Zujovic V. Multiple sclerosis patient macrophages impaired metabolism leads to an altered response to activation stimuli. Neurol Neuroimmunol Neuroinflamm. 2024;11(6): e200312.
• Köhler W, Engelen M, Eichler F, Lachmann R, Fatemi A, Sampson J, Salsano E, Gamez J, Molnar MJ, Pascual S, Rovira M, Vilà A, Pina G, Martín-Ugarte I, Mantilla A, Pizcueta P, Rodríguez-Pascau L, Traver E, Vilalta A, Pascual M, Martinell M, Meya U, Mochel F on behalf of the ADVANCE Study Group. Safety and efficacy of leriglitazone for preventing disease progression in men with adrenomyeloneuropathy (ADVANCE): a randomised, double-blind, multi-centre, placebo-controlled phase 2-3 trial. Lancet Neurol. 2023 Feb;22(2):127-136.