Demyelinating diseases, such as multiple sclerosis (MS), have a devasting impact on quality of live. A fundamental understanding of the causative mechanisms that drive demyelination, and disease progression, including remyelination failure, is currently lacking. In addition, myelin damage can occur as part of aging and is a common pathological feature of many neurological, including neurodegenerative diseases.
Our goal is to obtain insight in the molecular and cellular events driving myelin damage, and uncover molecular mechanisms that regulate interactions between neurons and glial cells crucial for myelination or responsible for remyelination failure upon myelin injury. By pinpointing key target mechanisms, we aim to design tools for therapeutic interventions.
We want to find druggable targets for demyelinating diseases like MS, aiming to develop means that selectively modulate the local pathogenic signalling environment to prevent lesion formation and/or halt disease progression. We have identified environmental signalling abnormalities in MS lesions, such as fibronectin aggregates and the persistent presence of neuronal galectin-4, that hamper remyelination. Currently, we devise and validate strategies that 1) prevent fibronectin aggregation, 2) degrade fibronectin aggregates or 3) reverse signal malfunctioning of fibronectin aggregates. We favor to develop therapeutics that cross the MS blood-brain barrier. Our research is integrated in Multiple Sclerosis Center Noord Nederland (MSCNN), a collaborative setting involving several MS research groups and patient care. The development of therapies to prevent demyelination or to aid remyelination is also of relevance for a range of other neurological diseases.
We investigate how the demyelinating disease MS affects myelin integrity and aim to understand cellular and molecular mechanisms that induce demyelination. We employ primary cell culture, organotypic slice cultures, hiPSC models and perform (ultrastructural) analysis on human CNS tissues.
We aim to understand why remyelination fails in MS by dissecting environmental signaling abnormalities taking diversity across CNS regions and MS lesions into account. We combine biochemical, molecular and omics analysis on primary cell culture, hiPSC model and (decellularized) human CNS tissue with functional assay in myelin-forming (MS) culture models.
We aim to translate our findings from basic research to therapeutic interventions. For promising therapeutic targets, we develop and validate tools to combat remyelination failure in MS.
Department of Biomedical Sciences of Cells and Systems
University Medical Center Groningen
Internal Zip code FB43
Antonius Deusinglaan, 1
9700 AD Groningen, The Netherlands
Visiting address
Myelin biology in disease
Wia Baron
Department of Biomedical Sciences of Cells and Systems
University Medical Center Groningen
Building 3215, 8th floor, room 0849
Antonius Deusinglaan, 1
9713 AV Groningen, The Netherlands
