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Publication : Prion protein (PrP) is not involved in the pathogenesis of spongiform encephalopathy in transgenic mice expressing interleukin-6 in the brain.

First Author  Castelnau PA Year  1997
Journal  Neurosci Lett Volume  234
Issue  1 Pages  15-8
PubMed ID  9347935 Mgi Jnum  J:137907
Mgi Id  MGI:3803389 Doi  10.1016/s0304-3940(97)00670-8
Citation  Castelnau PA, et al. (1997) Prion protein (PrP) is not involved in the pathogenesis of spongiform encephalopathy in transgenic mice expressing interleukin-6 in the brain. Neurosci Lett 234(1):15-8
abstractText  Transgenic mice expressing interleukin-6 (IL6) in the brain exhibit gliosis, spongiosis and neuronal loss. Based on previous findings, we hypothesized that IL6 could upregulate the prion protein (PrP) gene in the central nervous system (CNS) of these mice. Western and Northern blot analysis showed that PrP protein and mRNA levels were comparable to control levels. Furthermore, ultrastructural characterization revealed that spongiosis was actually located in astrocytes. These results indicate that IL6 does not upregulate the cerebral PrP expression in this animal model and that profound astrocytic alterations precipitate the neuronal degeneration observed.
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