Inflammatory Cyclooxygenase Activity and PGE₂ Signaling in Models of Alzheimer’s Disease

Title:Inflammatory Cyclooxygenase Activity and PGE₂ Signaling in Models of Alzheimer’s Disease

Volume: 11 Issue: 2

Author(s): Jenny U. Johansson, Nathaniel S. Woodling, Ju Shi and Katrin I. Andreasson

Affiliation:

Keywords: Alzheimer’s disease, microglia, amyloid beta, inflammation, cyclooxgenases, prostaglandin E₂, EP2 receptor, EP3 receptor, EP4 receptor.

Abstract: The inflammatory response is a fundamental driving force in the pathogenesis of Alzheimer’s disease (AD). In the setting of accumulating immunogenic Aß peptide assemblies, microglia, the innate immune cells of the brain, generate a non-resolving immune response and fail to adequately clear accumulating Aß peptides, accelerating neuronal and synaptic injury. Pathological, biomarker, and imaging studies point to a prominent role of the innate immune response in AD development, and the molecular components of this response are beginning to be unraveled. The inflammatory cyclooxygenase-PGE2 pathway is implicated in pre-clinical development of AD, both in epidemiology of normal aging populations and in transgenic mouse models of Familial AD. The cyclooxygenase-PGE₂ pathway modulates the inflammatory response to accumulating Aß peptides through actions of specific E-prostanoid G-protein coupled receptors.

Cite this article as:

Johansson U. Jenny, Woodling S. Nathaniel, Shi Ju and Andreasson I. Katrin, Inflammatory Cyclooxygenase Activity and PGE₂ Signaling in Models of Alzheimer’s Disease, Current Immunology Reviews (Discontinued) 2015; 11 (2) . https://dx.doi.org/10.2174/1573395511666150707181414