J
Jerome J. A. Hendriks
Researcher at University of Hasselt
Publications - 83
Citations - 3169
Jerome J. A. Hendriks is an academic researcher from University of Hasselt. The author has contributed to research in topics: Experimental autoimmune encephalomyelitis & Multiple sclerosis. The author has an hindex of 30, co-authored 74 publications receiving 2489 citations. Previous affiliations of Jerome J. A. Hendriks include VU University Amsterdam & Transnational University Limburg.
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Journal ArticleDOI
Tracking of myelin‐reactive T cells in experimental autoimmune encephalomyelitis (EAE) animals using small particles of iron oxide and MRI
Kurt Baeten,Peter Adriaensens,Jerome J. A. Hendriks,Evi Theunissen,Jan Gelan,Niels Hellings,Piet Stinissen +6 more
TL;DR: The study demonstrates the feasibility of tracking SPIO labelled myelin‐reactive T cells in the spinal cord as well as the brain of EAE rats upon systemic administration and provides data on the optimal labelling conditions for T cells leading to a high particle uptake and minimal aggregate formation.
Journal ArticleDOI
Effects of IFN-β, leptin and simvastatin on LIF secretion by T lymphocytes of MS patients and healthy controls
TL;DR: A reduced LIF production by CD4 + T cells of relapsing remitting MS patients as compared to healthy controls is reported and immunomodulatory agents such as leptin, IFN-β and simvastatin were studied for their potential to alter LIF and secretion of other cytokines by T cells and monocytes.
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Changes in characteristics of rat skeletal muscle after experimental allergic encephalomyelitis
TL;DR: The data suggest that, as a result of central neuroinflammatory diseases, maximal performance of skeletal muscle is impaired but submaximal performance is relatively well maintained.
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Low-Density Lipoprotein Receptor Deficiency Attenuates Neuroinflammation through the Induction of Apolipoprotein E.
Jo Mailleux,Silke Timmermans,Katherine Nelissen,Jasmine Vanmol,Tim Vanmierlo,Jack van Horssen,Jeroen F. J. Bogie,Jerome J. A. Hendriks +7 more
TL;DR: Findings show that LDLr and associated apoE levels are involved in neuroinflammatory processes and that ldlr−/− reduces EAE disease severity in female but not in male EAE mice, and that this can be explained by increased levels of apOE in female ldLR−/ − mice.
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Advanced Glycation Endproducts Are Increased in the Animal Model of Multiple Sclerosis but Cannot Be Reduced by Pyridoxamine Treatment or Glyoxalase 1 Overexpression.
Suzan Wetzels,Suzan Wetzels,Kristiaan Wouters,Toshio Miyata,Jean L.J.M. Scheijen,Jerome J. A. Hendriks,Casper G. Schalkwijk,Tim Vanmierlo,Tim Vanmierlo +8 more
TL;DR: AGEs levels increase during EAE in the spinal cord, but AGE-modifying treatments do not inhibit EAE-induced AGE production and do not affect disease progression.