Microarray analysis of the in vivo response of microglia to Aβ peptides in mice with conditional deletion of the prostaglandin EP2 receptor.

ABSTRACT: Amyloid-β (Aβ) peptides accumulate in the brains of patients with Alzheimer's disease (AD), where they generate a persistent inflammatory response from microglia, the innate immune cells of the brain. The immune modulatory cyclooxygenase/prostaglandin E2 (COX/PGE₂) pathway has been implicated in preclinical AD development, both in human epidemiology studies¹ and in transgenic rodent models of AD^{2, 3}. PGE₂ signals through four G-protein-coupled receptors, including the EP2 receptor that has been investigated for its role in mediating the inflammatory and phagocytic responses to Aβ⁴. To identify transcriptional differences in microglia lacking the EP2 receptor, we examined mice with EP2 conditionally deleted in Cd11b-expressing immune ce

SUBMITTER: Johansson JU 

PROVIDER: S-EPMC4522932 | biostudies-literature | 2015 Sep

REPOSITORIES: biostudies-literature