期刊
JOURNAL OF NEUROIMMUNOLOGY
卷 164, 期 1-2, 页码 85-92出版社
ELSEVIER
DOI: 10.1016/j.jneuroim.2005.04.002
关键词
thiamine; neurodegeneration; oxidative stress; inflammation; CD40
资金
- NIA NIH HHS [AG11921, AG14600, AG14930] Funding Source: Medline
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 CD40L-/- mice. CD40L-/- 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. (C) 2005 Elsevier B.V. All rights reserved.
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