Immunohistochemical Characterisation of Classical Scrapie Neuropathology in Sheep

• Published in: Journal of comparative pathology 2009-08, Vol.141 (2), p.135-146
• Main Authors: Vidal, E., Acín, C., Foradada, L., Monzón, M., Márquez, M., Monleón, E., Pumarola, M., Badiola, J.J., Bolea, R.
• Format: Article
• Language: English
• Subjects: Animals; Astrocytes - metabolism; Astrocytes - pathology; biomarkers; Biomarkers - metabolism; brain; Brain - metabolism; Brain - pathology; central nervous system; Female; Fluorescent Antibody Technique, Direct - veterinary; Heat-Shock Proteins - metabolism; histochemistry; histopathology; immunohistochemistry; Metallothionein - metabolism; Microglia - metabolism; Microglia - pathology; neuroglia; neuroinflammation; Oxidative Stress - physiology; pathogenesis; prion; protein deposition; PrPSc deposition; PrPSc proteins; PrPSc Proteins - metabolism; scrapie; Scrapie - metabolism; Scrapie - pathology; Sheep; Vimentin - metabolism
• ISSN: 0021-9975; 1532-3129
• DOI: 10.1016/j.jcpa.2009.04.002

Neuroinflammation elicited by PrP res (resistant prion protein [PrP]) deposits in the central nervous system (CNS) has been shown to involve cellular and oxidative stress responses in bovine spongiform encephalopathy (BSE) as well as in several murine models of transmissible spongiform encephalopathy (TSE). Additionally, deregulation of water homeostasis has been suggested to be a further component of the spongiform changes observed in TSEs. The aim of the present study was to characterize the pathogenic events occurring in the CNS of sheep with spontaneously arising classical scrapie. Brains from seven affected animals and two controls were subject to immunohistochemical and histochemical examinations. Semi-quantitative evaluation of PrP res deposits and spongiform changes throughout the encephalon confirmed that PrP res deposition elicits significant astroglial and microglial reactions, as evidenced by an increase in the number of glial cells and changes in glial cell morphology involving increased expression of vimentin. The altered expression of metallothionein and heat shock protein 25 (HSP25) suggested that this neuroinflammatory reaction entails cellular and oxidative stress responses. In contrast, there was no change in expression of the membrane-associated water channel aquaporin 1 when PrP res accumulated in the brain.