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Jeroen F. J. Bogie

Researcher at University of Hasselt

Publications -  49
Citations -  1582

Jeroen F. J. Bogie is an academic researcher from University of Hasselt. The author has contributed to research in topics: Myelin & Experimental autoimmune encephalomyelitis. The author has an hindex of 20, co-authored 40 publications receiving 1030 citations. Previous affiliations of Jeroen F. J. Bogie include Rotterdam University of Applied Sciences & Transnational University Limburg.

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Macrophage subsets and microglia in multiple sclerosis.

TL;DR: It is concluded that microglia and macrophages are highly dynamic cells displaying disease stage and location-specific fates in neurological disorders, and changing the physiology of divergent phagocyte subsets at particular disease stages holds promise for future therapeutics for CNS pathologies.
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High Fat Diet Exacerbates Neuroinflammation in an Animal Model of Multiple Sclerosis by Activation of the Renin Angiotensin System

TL;DR: The data show that diets containing excess fat have a significant influence on neuroinflammation in EAE, which may have important implications for the treatment and prevention of neuroinflammatory disorders.
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The physiology of foamy phagocytes in multiple sclerosis.

TL;DR: This review summarizes and discusses the current knowledge on the spatiotemporal physiology of foamy phagocytes in MS lesions, and elaborate on extrinsic and intrinsic factors regulating their behavior.
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Selective identification of macrophages and cancer cells based on thermal transport through surface-imprinted polymer layers.

TL;DR: A novel straightforward method for the specific identification of viable cells and cancer cells with their respective imprints in a buffer solution based on changes of the heat transfer resistance at the solid-liquid interface of a thermal sensor device induced by binding of the cells to a surface-imprinted polymer layer covering an aluminum chip.
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CD36-mediated uptake of myelin debris by macrophages and microglia reduces neuroinflammation.

TL;DR: Evidence is provided that CD36 is crucial for clearing myelin debris and suppressing neuroinflammation in demyelinating disorders such as MS by using the EAE model, and that it markedly increased the neuroinflammatory burden and disease severity in the Eae model.