Rezaie, P. and Lantos, P.L.
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|DOI (Digital Object Identifier) Link:||http://doi.org/10.1016/S0165-0173(01)00042-X|
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Alterations in the phenotype and function of microglia, the resident mononuclear phagocytes of the central nervous system, are among the earliest indications of pathology within the brain and spinal cord. The prion diseases, also known as spongiform encephalopathies, are fatal neurodegenerative disorders with sporadic, genetic or acquired infectious manifestations. A hallmark of all prion diseases is the aberrant metabolism and resulting accumulation of the prion protein. Conversion of the normal cellular protein [PrP(c)] into the abnormal pathogenic (or disease-causing) isoform [PrP(Sc)] involves a conformational alteration whereby the alpha-helical content is transformed into beta-sheet. The histological characteristics of these disorders are spongiform change, astrocytosis, neuronal loss and progressive accumulation of the protease-resistant prion isoform. An additional upregulation in microglial response has been reported in Kuru, Creutzfeldt-Jakob disease (CJD), Gerstmann-Straussler-Scheinker syndrome (GSS), scrapie, in transgenic murine models and in culture, where microglial activation often accompanies prion protein deposition and neuronal loss. This article will review the roles of microglia in spongiform encephalopathies.
|Item Type:||Journal Article|
|Academic Unit/Department:||Science > Life, Health and Chemical Sciences
|Interdisciplinary Research Centre:||Biomedical Research Network (BRN)|
|Depositing User:||Payam Rezaie|
|Date Deposited:||14 Jun 2006|
|Last Modified:||14 Jan 2016 15:48|
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Microglia and the pathogenesis of spongiform encephalopathies. (deposited 14 Jun 2006)
- Microglia and the pathogenesis of spongiform encephalopathies. (deposited 14 Jun 2006) [Currently Displayed]