CD45 deficiency drives amyloid-β peptide oligomers and neuronal loss in Alzheimer's disease mice.

@article{Zhu2011CD45DD,
  title={CD45 deficiency drives amyloid-β peptide oligomers and neuronal loss in Alzheimer's disease mice.},
  author={Yuyan Zhu and Huayan Hou and Kavon Rezai-zadeh and Brian Giunta and Amanda Ruscin and Carmelina Gemma and Jingji Jin and Natasa B Dragicevic and Patrick Terrence Bradshaw and Suhail Rasool and Charles G. Glabe and Jared Ehrhart and Paula C Bickford and Takashi Mori and Demian F. Obregon and Terrence C. Town and Jun Tan},
  journal={The Journal of neuroscience : the official journal of the Society for Neuroscience},
  year={2011},
  volume={31 4},
  pages={1355-65}
}
Converging lines of evidence indicate dysregulation of the key immunoregulatory molecule CD45 (also known as leukocyte common antigen) in Alzheimer's disease (AD). We report that transgenic mice overproducing amyloid-β peptide (Aβ) but deficient in CD45 (PSAPP/CD45(-/-) mice) faithfully recapitulate AD neuropathology. Specifically, we find increased abundance of cerebral intracellular and extracellular soluble oligomeric and insoluble Aβ, decreased plasma soluble Aβ, increased abundance of… CONTINUE READING
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