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Prof. Dr. Vincent van Pesch and his team

The neuroinflammatory role of micro-RNAs in extracellular vesicles: biomarkers and therapeutic tools for the immune dysregulation in Multiple Sclerosis

Grant

€ 30,000 / 2 years
Unit of Neurochemistry- Cliniques Universitaires St Luc
“This project aims to study the involvement of circulating extracellular vesicles and micro-RNAs in neuroinflammation, to decipher MS pathogenesis and generate novel therapeutic strategies.”

The pathogenesis of Multiple Sclerosis (MS), an immune-mediated disorder of the central nervous system, is still incompletely understood. Our research aims to study recently discovered biological regulators, microRNAs, which circulate in bodily fluids in spherical lipidic structures called exosomes. We aim to study the expression profile of microRNAs, characterize their carriers (exosomes) in the cerebrospinal fluid and blood from MS patients, determine their cellular source and study how they regulate the inflammatory response, during the relapsing and progressive phase of the disease. This will unravel novel biological pathways involved in MS pathogenesis and could help identify novel therapeutic targets.

the scientific project

The challenge in designing more effective treatments for Multiple Sclerosis (MS) resides in its complex and incompletely understood pathogenesis. It is therefore important to characterize novel bioactive molecules that could play a role in the inflammatory or neurodegenerative aspects of the disease. Cell-to-cell communication can occur through exosomes containing micro-RNAs. MiRNAs are small non-coding genetic material, able to regulate hundreds of genes. Several miRNAs have been associated with MS, but their cellular source and biological activity remain mostly uncharacterized. The aim of this innovative project is to characterize, both phenotypically and functionally, the effects of the combination of miRNA and EVs on the immune dysregulation in MS, leading to the discovery of novel signalling pathways and therapeutic targets.