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- W2000912470 abstract "Abstract: One increasingly dominant hypothesis regarding the pathogenesis of Alzheimer dementia is the inflammationhypothesis. In brief, this hypothesis argues that at least some of the neurodegeneration found in this disease issecondary to excessive activation of microglia and astrocytes, resulting in secretion of pro-inflammatory mediators,activation of the complement cascade and degeneration of synapses and neurons. The APP+PS1 transgenic mouse isa model of As amyloid deposition that results in a phenotype resembling some but not all aspects of Alzheimer's. Ourgroup has evaluated a number of manipulations designed to both exacerbate and ameliorate the microglial activationin this transgenic model, ranging from LPS injections, administration of anti-As antibodies and treatment with anti-inflammatory drugs. Contrary to our original predictions that microglial activation should exacerbate the Alzheimerphenotype in these mice, we find that treatments that cause microglial activation are associated with reduced amyloidloads. These data are discussed in the context of differences between the murine and human immune systems andqualitative differences in the As deposits found in these mouse models compared to human specimens." @default.
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- W2000912470 date "2003-03-01" @default.
- W2000912470 modified "2023-09-25" @default.
- W2000912470 title "The Association of Microglial Activation and Amyloid Reduction in APP+PS1 Transgenic Mice" @default.
- W2000912470 doi "https://doi.org/10.2174/1568013033358680" @default.
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