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Project

Targeting disturbed lipophagy promotes remyelination in multiple sclerosis (R-9979)

Multiple sclerosis (MS) is a neurodegenerative autoimmune disease of the central nervous system (CNS) in which microglia and infiltrated macrophages play a crucial role. Driving these phagocytes towards an anti-inflammatory and regenerative phenotype is considered a promising strategy to halt MS disease progression. Despite being the most abundant cell type in MS lesions, the impact that myelincontaining phagocytes have on MS lesion progression remains largely unclear. Our preliminary data now indicate that prolonged intracellular accumulation of myelin-derived lipids skews phagocytes towards a disease-promoting phenotype. Moreover, we found that lipophagy, a mechanism that helps degrade cellular lipid content, is implicated in the induction of this phenotype. By using wellestablished animal models for neuroinflammation and CNS repair, I unravel in this project whether targeting lipophagy represents a promising therapeutic intervention for MS. Furthermore, I define whether impaired lipophagy also drives the phenotype of human phagocytes upon myelin uptake and unravel the molecular mechanisms that underlie the degradation of lipid droplets by lipophagy in myelin-containing phagocytes. Obtained results will lead to increased insight into MS lesion development and repair, and identify lipophagy inducers as a promising therapeutic intervention for MS.
Date:1 Oct 2019 →  30 Oct 2019
Keywords:MULTIPLE SCLEROSIS
Disciplines:Autoimmunity, Cell signalling, Neurosciences not elsewhere classified