DISCOVER THE HENDRIKS MIND LAB

During MS, macrophages infiltrate the brain and together with microglia, the resident immune cells of the CNS, degrade myelin, an insulating layer surrounding nerves that is important for the propagation of action potentials.  Myelin breakdown, also called demyelination, leads to failure of nerve conduction and to a wide range of clinical symptoms such as loss of vision and muscle weakness. Besides contributing to demyelination, macrophages and microglia can also promote repair of damaged tissue (remyelination) by clearing myelin debris and secreting anti-inflammatory and neurotrophic factors.

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Myelin consists for the major part of lipids, such as cholesterol and fatty acids. In MS, a disturbed lipid metabolism is detected. However, little is known about the cause of this disturbance and the impact it has on disease progression. Our findings show that lipids present in myelin alter the function of macrophages and microglia. By targeting the underlying pathways, a beneficial macrophage/microglia phenotype can be induced that slows down lesion progression and stimulates repair. Interestingly, specific nutritional components impact lipid metabolism and immune cell function and thus provide a promising strategy to limit lesion progression and promote CNS repair.

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Our research aims at elucidating metabolic pathways which underly disruptions in these cellular processes, with the goal to identify new interesting targets for future therapeutic applications. Furthermore, we study the impact of specific nutritional components on lesion progression an CNS repair, as they were demonstrated to control lipid metabolism and immune cell function.

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Specifically, we aim to: