Glia as a therapeutic target: selective suppression of human amyloid-beta-induced upregulation of brain proinflammatory cytokine production attenuates neurodegeneration.

@article{Ranaivo2006GliaAA,
  title={Glia as a therapeutic target: selective suppression of human amyloid-beta-induced upregulation of brain proinflammatory cytokine production attenuates neurodegeneration.},
  author={Hantamalala Ralay Ranaivo and Jeffrey Craft and Wenhui Hu and Ling Guo and Laura K Wing and Linda J. Van Eldik and D Martin Watterson},
  journal={The Journal of neuroscience : the official journal of the Society for Neuroscience},
  year={2006},
  volume={26 2},
  pages={662-70}
}
A corollary of the neuroinflammation hypothesis is that selective suppression of neurotoxic products produced by excessive glial activation will result in neuroprotection. We report here that daily oral administration to mice of the brain-penetrant compound 4,6-diphenyl-3-(4-(pyrimidin-2-yl)piperazin-1-yl)pyridazine (MW01-5-188WH), a selective inhibitor of proinflammatory cytokine production by activated glia, suppressed the human amyloid-beta (Abeta) 1-42-induced upregulation of interleukin… CONTINUE READING