The Journal of Neuroscience, November 2, 2005, ():
Deletion of the Prostaglandin E2 EP2 Receptor Reduces Oxidative Damage and Amyloid Burden in a Model of Alzheimer's Disease
J. Neurosci. Liang et al.
25: 10180
Supplemantal data
Files in this Data Supplement:
- supplemental material
-
Supplemental Figure 5. Model of PGE2 EP2 receptor function in APPSwe-PS1?E9 mice. EP2 receptor is present on microglia (light blue cell) and activation of the EP2 receptor (in red) by PGE2 leads to an increase in the production of microglial superoxides and neurotoxins (1). Increased production of reactive oxygen species promotes lipid peroxidation and injury in neurons (gray cell), as measured by F4 neuroprostanes; this oxidative stress induces BACE1 enzymatic activity (2) and cleavage of APP to generate higher levels of ß-CTF. Increased levels of ß-CTF are processed to Aß peptides by ?-secretase complex, and production and/or fibrillization of these Aß peptides leads to further inflammation, induction of COX enzymatic activity, and PGE2 production (3); increased PGE2 levels in turn further activate microglial EP2 receptors to perpetuate and amplify the cycle.
