Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
9194734 | Journal of Neuroimmunology | 2005 | 8 Pages |
Abstract
Inflammatory/immune processes are important in the pathogenesis of neurodegenerative diseases. Thiamine deficiency (TD) models the region selective neuronal loss in brain that accompanies mild impairment of oxidative metabolism. TD induces well-defined alterations in neurons, microglia, astrocytes, and endothelial cells. To test the role of inflammatory/immune mechanisms in TD-induced neurodegeneration, the temporal profile of neurodegeneration was compared to the activation of CD68-positive microglia and ICAM-1-positive endothelial cells during TD in wild type mice and in CD40Lâ/â mice. CD40Lâ/â delayed the onset of TD-induced neuronal death as well as the activation of microglia and endothelial cells. The current results suggest that CD40L-mediated immune and inflammatory responses have a role in TD-induced neuronal death.
Keywords
FJBSmTNHeme oxygenase-1Fluoro-Jade BKPBSCD40DABNeuNEAEAPCeNOSHO-1ICAM-13,3′-diaminobenzidineBSAbovine serum albuminAntigen presenting cellsexperimental autoimmune encephalomyelitisinflammationOxidative stressNeurodegenerationThiaminemammillothalamic tractendothelial nitric oxide synthaseintercellular adhesion molecule-1Mediodorsal thalamic nucleusventrolateral thalamic nucleusventromedial thalamic nucleuspotassium phosphate-buffered salineneuronal specific nuclear proteinthiamine deficiency
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Authors
Zun-Ji Ke, Noel Y. Calingasan, Saravanan S. Karuppagounder, Lorraine A. DeGiorgio, Bruce T. Volpe, Gary E. Gibson,