Abstract
Tumor necrosis factor (TNF) mediates chronic inflammatory pathologies including those affecting the central nervous system (CNS), but non-selective TNF inhibitors exacerbate multiple sclerosis (MS) and TNF receptor SF1A is associated with MS, indicating beneficial effects of TNF in CNS pathology. In this study, we compared the effects of soluble (solTNF) and transmembrane TNF (tmTNF) in a mouse model of chronic MS induced by oral administration of the neurotoxin cuprizone (CPZ). In this model disease is compartmentalized behind an intact blood brain barrier (BBB) and monitored by widespread activation and proliferation of microglia, astrocytes and oligodendrocyte precursor cells (OPC) after 2weeks of CPZ and progressive demyelination and neurodegeneration, most obvious in the corpus callosum, with maximum lesions being observed at 5weeks of administration.
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