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- W1972938215 endingPage "72" @default.
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- W1972938215 abstract "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 [PrPc] into the abnormal pathogenic (or disease-causing) isoform [PrPSc] involves a conformational alteration whereby the α-helical content is transformed into β-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–Sträussler–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." @default.
- W1972938215 created "2016-06-24" @default.
- W1972938215 creator A5006054229 @default.
- W1972938215 creator A5012877366 @default.
- W1972938215 date "2001-03-01" @default.
- W1972938215 modified "2023-10-11" @default.
- W1972938215 title "Microglia and the pathogenesis of spongiform encephalopathies" @default.
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