Charcot Fellowship

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Faithful to its mission to serve the public interest in the field of fundamental and  translational research, the Charcot Foundation has set up the Charcot Fellowship, a programme of doctoral grants for young researchers (under 30). The grant will enable them to do four years of research dedicated to MS and make advances in the fight against the disease. The goal of the grants is to strengthen the research potential of teams in Belgium interested in multiple sclerosis. By involving young researchers who want to do their doctoral thesis on multiple sclerosis, the grant is intended to have a long-term impact on research to defeat the disease.

Charcot Fellowship 2016-2020: Elien Grajchen (UHasselt)

Photo: The research group of Prof. Hendriks; Charcot Fellowship 2016-2020. Dr. Jeroen Bogie (co-promoter), Fellow Elien Grajchen, Prof. Dr. Jerome Hendriks (promoter) - UHasselt.

The first scholar is Mrs Elien GRAJCHEN (UHasselt), whose promoter is Prof. Dr Jerome HENDRIKS, Associate Professor of Immunology and Biochemistry, Institute for Biomedical Research, University of Hasselt. The choice of Mrs GRAJCHEN confirms the quality of the current UHasselt research team and will encourage young people to embark on studies or a scientific career.

Multiple sclerosis is characterized by excessive infiltration of myeloid cells in the central nervous system. Until recently, myeloid cells present in demyelinated plaques were only thought to promote neuroinflammation and neurodegeneration by secreting cytotoxic inflammatory mediators and engulfing the protective myelin. However, recent studies have reported that macrophages can also have beneficial functions in multiple sclerosis (MS) as myelin uptake skews macrophages towards a more wound healing phenotype. Strikingly, our preliminary data suggest that prolonged myelin internalization reshapes the macrophages to a more inflammatory phenotype. The exact mechanism underlying this inflammatory phenotype switch remains unclear, but our preliminary data indicate that an enzyme involved in fatty acid metabolism plays an important role. During my PhD, I will elucidate how this enzyme is involved in the myelin-induced changes in the macrophage phenotype and discover new targets for the development of new and better therapies that can diminish neuroinflammation and improve tissue repair.

The research group of Prof Hendriks aims to elucidate the impact of a disturbed lipid metabolism on inflammatory and repair processes in multiple sclerosis (MS). During MS, infiltrated macrophages and microglia degrade the myelin sheath surrounding axons, so called demyelination. As myelin is essential for axonal conduction, demyelination leads to conduction failure and clinical symptoms such as loss of vision and muscle weakness. Myelin consists for the major part of lipids of which some, such as cholesterol and fatty acids, also have important immune regulatory functions. In MS, a disturbed cholesterol and fatty acid metabolism is observed. However, little is known about the cause of this disturbance and the impact it has on disease progression. The group of Prof Hendriks determines the involvement of cholesterol and fatty acids in central nervous system (CNS) inflammation, demyelination and repair of damaged myelin sheaths. Interestingly, certain dietary components can affect CNS lipid metabolism and the function of resident brain cells. Therefore, another line of research is aimed at establishing the impact of dietary components on disease progression in MS.