NR AUSB
AU Bahlo,A.; Lindner,N.; Flechsig,E.; Klein,M.A.
TI Unaltered neurodegeneration in prion-infected neurografts devoid of BCL-2 or BAX
QU TSE-Forum, 6. Kongress - Nationale TSE-Forschungsplattform, Greifswald 26.6.-28.6.2006, Poster: Pathogenese/Infektion PATH-02
PT Konferenz-Poster
AB The mechanisms of neuronal apoptosis and neurodegeneration in prion diseases or transmissible spongiform encephalopathies (TSE) are still unresolved. Histopathological changes such as microvacuolation (spongiosis) and reactive gliosis are typically found in the brain and are accompanied by PrP-immunoreactive deposits within dendrites and cell bodies of neurons and by neuronal cell loss. Prion-induced neuronal cell death appears to be associated with apoptosis. Expression levels of the apoptotic proteins like BAX and BCL-2 are altered in hippocampal neurons of infected hamsters. An antiapoptotic function against BAX induced apoptosis has been postulated for PrPc and binding of PrPc to the C-terminus of BCL-2 has been shown in a yeast-two-hybrid screen. To further characterize the role of BAX and BCL-2 in prion-mediated neurodegeneration in vivo, we transplanted BAX- and BCL-2-deficient neuroectodermal tissue in the brain of Prnpo/o recipient mice. After long-term infection with mouse scrapie prions, typical histopathological features of the disease, such as gliosis, spongiosis and PrPsc accumulation were found strictly restricted to the neurografts. Our studies indicate that BAX and BCL-2 are not directly involved in the mechanisms leading to the neurodegeneration in prion disease.
AD Angela Bahlo, Nele Lindner, Eckhard Flechsig and Michael A. Klein, Institute of Virology, University of Wuerzburg, Wuerzburg, Germany
SP englisch
PO Deutschland
OR Tagungsband