학술논문
Inflammatory Cyclooxygenase Activity and PGE 2 Signaling in Models of Alzheimer's Disease.
Document Type
Academic Journal
Author
Johansson JU; Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA 94305, USA.; Present address: SRI International, Menlo Park, CA, USA.; Woodling NS; Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA 94305, USA.; Present address: Institute of Healthy Ageing, University College London, London, UK.; Shi J; Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA 94305, USA.; Present address: True North Therapeutics, South San Francisco, CA, USA.; Andreasson KI; Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA 94305, USA.
Source
Publisher: Bentham Science Publishers Country of Publication: United Arab Emirates NLM ID: 101253279 Publication Model: Print Cited Medium: Print ISSN: 1573-3955 (Print) Linking ISSN: 15733955 NLM ISO Abbreviation: Curr Immunol Rev Subsets: PubMed not MEDLINE
Subject
Language
English
ISSN
1573-3955
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-PGE 2 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-PGE 2 pathway modulates the inflammatory response to accumulating Aß peptides through actions of specific E-prostanoid G-protein coupled receptors.