Microglial response to A? and prostaglandin-E2 EP4 receptor activation

ABSTRACT: A persistent and non-resolving inflammatory response to accumulating A? peptide species is a cardinal feature in the development of Alzheimer's disease (AD). In response to accumulating A? peptide species, microglia, the innate immune cells of the brain, generate a toxic inflammatory response that accelerates synaptic and neuronal injury. Many pro-inflammatory signaling pathways are linked to progression of neurodegeneration. However, endogenous anti-inflammatory pathways capable of suppressing A?-induced inflammation represent a relatively unexplored area. Here we hypothesized that signaling through the prostaglandin-E2 (PGE2) EP4 receptor potently suppresses microglial inflammatory responses to A?42 peptides. In cultured microglial cells, EP4 stimulation attenuated levels of A?42-induced

ORGANISM(S): Mus musculus

SUBMITTER: Katrin Andreasson 

PROVIDER: E-GEOD-55627 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress