Professor Elga de Vries received her PhD in 1995 in the field of Pharmacology, focussing on the identification of altered function of the cerebral vasculature and glial cells in the disease state to determine novel ways to deliver drugs into the central nervous system.
Subsequently, she became a Marie Curie post-doctoral research fellow at University College London, United Kingdom, studying signalling events in brain endothelial cells under inflammatory conditions. In 2011, she became a full professor of neuro-immunology at the Department of Molecular Cell Biology and Immunology at the MS Center Amsterdam, the Netherlands.
She is currently principal investigator of the neuro-immunology research group and her main research interests are the understanding of underlying molecular mechanisms of MS disease progression, with a focus on altered glial response and vascular function.
Dynamics of M1/M2 polarization of microglia in multiple sclerosis: a PET imaging study
Neuroinflammation and neurodegeneration as observed in multiple sclerosis (MS) have many different aspects and facets. However, a central characteristic is the activation of microglia, a diverse process manifesting in distinct activation types, depending on type and phase of pathology. The complex molecular and cellular processes accompanying microglia activation are highly dynamic and may contribute to tissue damage, neurodegeneration and brain dysfunction. Once activated, microglia can adopt diverse phenotypes ranging between two extremes: a classically activated M1 phenotype that is involved in pro-inflammatory actions and an alternatively activated M2 phenotype that is mainly involved in anti-inflammatory actions and tissue repair.
As microglia play an important role in the progression of MS, the development of novel treatments to halt neurodegeneration may be by skewing the polarization state of microglia to the more protective phenotype. To date, no insights into their polarization status in patients exist due to a lack of diagnostic in vivo tools. Within the current research proposal we will use a recently developed M2 specific Positron Emission Tomography (PET) tracer, binding to the purinergic receptor P2X7, to assess polarization of activated microglia experimentally in in vivo models. We will further determine tracer specificity in human post-mortem tissues, define binding to the M2 status of microglia cells and correlate the expression to neurodegeneration. Finally, we will conduct the first human studies to obtain essential insights into the dynamics of M1/M2 phenotypes in patients with MS.
Ultimately, microglia phenotype imaging will offer a unique opportunity to study the mechanism of action of novel drugs and is aimed at preventing neurodegeneration by modulating microglia activation and stimulating neuroprotection in patients with progressive MS.
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