Submit Manuscript  

Article Details

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

[ Vol. 11 , Issue. 2 ]


Jenny U. Johansson, Nathaniel S. Woodling, Ju Shi and Katrin I. Andreasson   Pages 125 - 131 ( 7 )


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.


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


Stanford University School of Medicine, 1201 Welch Road, Stanford, CA 94305, USA.

Read Full-Text article