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

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

Journal Name: Current Immunology Reviews (Discontinued)

Volume 11 , Issue 2 , 2015


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.

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

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Article Details

Year: 2015
Page: [125 - 131]
Pages: 7
DOI: 10.2174/1573395511666150707181414

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