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Bart J.L. Eggen on Muck Rack

Bart J.L. Eggen

As seen in: BioRxiv, Cell Press
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Articles

Temporal changes in metabolism guide oligodendrocyte precursor cell dynamics in aging and multiple sclerosis

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By Tess Dierckx, Sarah Wilson, Rebecca Buchanan, Themistoklis M. Tsarouchas, Yuhsiang Cheng, Maria Nunez, Kelly Strickland, Dena Kumsa, Yohan S.S. Auguste, Sam Vanherle, Sander Bouwman, Daniela Rojo, Louisa Dal Cengio, Celia Lerma-Martin, Yassene Mohammed, Lucas Schirmer, Jeroen F.J. Bogie, Bart J.L. Eggen, Erin Gibson
| Cell Press Verified
Keywords oligodendrocytes myelination oligodendrocyte precursor cells OPCs multiple sclerosis metabolism aging circadian BMAL1 iPSC Introduction The age-associated failure to generate oligodendrocytes through oligodendrocyte precursor cell (OPC) differentiation contributes to the aging-related decline in myelin capacity.1,2 How aging drives these OPC deficits remains incompletely understood.
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Microglial lipid phosphatase SHIP1 limits complement-mediated synaptic pruning in the healthy developing hippocampus

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By Alessandro Matera, Anne-Claire Compagnion, Chiara Pedicone, M. Janssen, Andranik Ivanov, Katia Monsorno, Gwenaël Labouèbe, Loredana Leggio, Marta Pereira, Dieter Beule, Virginie Mansuy-Aubert, Tim Williams, Nunzio Iraci, Amanda Sierra, Samuele G. Marro, Alison Goate, Bart J.L. Eggen, WILLIAM Kerr, Rosa C. Paolicelli
| Cell Press Verified
Keywords microglia INPP5D SHIP1 synaptic pruning complement Alzheimer’s disease AD risk genes cognitive dysfunction Introduction Inositol polyphosphate-5-phosphatase D (INPP5D) encodes for SH2-containing inositol polyphosphate 5-phosphatase 1 (SHIP1).
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Microglial states determine lesion dynamics in multiple sclerosis

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By Jia Hui Khoo, Zhigang Lu, Dennis D. Wever, Bart J.L. Eggen
| BioRxiv
Abstract Multiple sclerosis (MS) is a neuroinflammatory disease of the central nervous system, characterized by demyelinating lesions 1. Lesion expansion contributes to progression and increased disability, while remyelination can recover neurological deficits. However, mechanisms driving lesion dynamics are largely unclear, hindering the development of effective therapeutics. We propose that distinct states of microglia are involved in lesion expansion and remyelination 2,3.
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