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10.1111/j.1460-9568.2006.05069.x

http://scihub22266oqcxt.onion/10.1111/j.1460-9568.2006.05069.x
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17067295!ä!17067295

suck abstract from ncbi


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pmid17067295      Eur+J+Neurosci 2006 ; 24 (7): 1923-34
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  • Viral-induced inflammation is accompanied by beta-amyloid plaque reduction in brains of amyloid precursor protein transgenic Tg2576 mice #MMPMID17067295
  • Stahl T; Reimers C; Johne R; Schliebs R; Seeger J
  • Eur J Neurosci 2006[Oct]; 24 (7): 1923-34 PMID17067295show ga
  • Amyloid plaques, one of the neuropathological hallmarks of Alzheimer's disease, and their main constituent, the amyloid beta-peptide (Abeta), are triggers of the activation of innate inflammatory mechanisms involving the activation of microglia. To dissect the effects of a non-Abeta-specific microglial activation on the Abeta metabolism, we employed a viral infection-based model. Transgenic mice expressing a mutated form of the human amyloid precursor protein (Tg2576) were used. In preceding experiments, 2-week-old transgenic mice and non-transgenic littermates were infected intracerebrally with the neurotropic Borna disease virus and investigated at 2, 4 and 14 weeks post-infection. The Borna disease virus-inoculated mice showed a persisting, subclinical infection of cortical and limbic brain areas characterized by slight T-cell infiltrates, expression of cytokines and a massive microglial activation in the hippocampus and neocortex. Viral-induced effects reached their peak at 4 weeks post-infection. In 14-month-old Tg2576 mice, characterized by the deposition of diffuse and dense-core amyloid plaques in cortical brain regions, Borna disease virus-induced microglial activation in the vicinity of Abeta deposits was used to investigate the influence of a local inflammatory response on these deposits. At 4 weeks post-infection, histometric analyses employing Abeta immunohistochemistry revealed a decrease of the cortical and hippocampal Abeta-immunopositive area. This overall decrease was accompanied by a decrease of parenchymal thioflavin-S-positive amyloid deposits and an increase of such deposits in the walls of cerebral vessels, which indicates that the elicitation of a non-Abeta-specific microglial activation may contribute to a reduction of Abeta in the brain parenchyma.
  • |*Borna disease virus[MESH]
  • |Amyloid beta-Protein Precursor/genetics[MESH]
  • |Animals[MESH]
  • |Animals, Newborn[MESH]
  • |Benzothiazoles[MESH]
  • |Brain/*metabolism/pathology/*virology[MESH]
  • |Cytokines/genetics/metabolism[MESH]
  • |Electrophoresis, Polyacrylamide Gel/methods[MESH]
  • |Electrophoretic Mobility Shift Assay/methods[MESH]
  • |Gene Expression/physiology[MESH]
  • |Glial Fibrillary Acidic Protein/metabolism[MESH]
  • |Humans[MESH]
  • |Immunohistochemistry/methods[MESH]
  • |Inflammation/*metabolism/*virology[MESH]
  • |Mice[MESH]
  • |Mice, Inbred C57BL[MESH]
  • |Mice, Transgenic[MESH]
  • |Neuroglia/metabolism/pathology[MESH]
  • |Nucleoproteins/metabolism[MESH]
  • |Plaque, Amyloid/*pathology[MESH]
  • |T-Lymphocytes/metabolism/pathology[MESH]
  • |Thiazoles[MESH]
  • |Time Factors[MESH]


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