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

[ Vol. 11 , Issue. 2 ]

Author(s):

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

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.

Keywords:

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

Affiliation:

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



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