Journal
CURRENT MEDICINAL CHEMISTRY
Volume 15, Issue 19, Pages 1863-1869Publisher
BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/092986708785132915
Keywords
prostaglandins; PGE2; CNS; neurodegeneration; EP receptors
Funding
- NIA NIH HHS [P50 AG005136, P50 AG005136-239003] Funding Source: Medline
- NIGMS NIH HHS [P01 GM015431, P50 GM015431, P50 GM015431-390002] Funding Source: Medline
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Prostaglandins (PGs) are potent autocrine and paracrine oxygenated lipid molecules that contribute appreciably to physiologic and pathophysiologic responses in almost all organs, including brain. Emerging data indicate that the PGs, and more specifically PGE(2), play a central role in brain diseases including ischemic injury and several neurodegenerative diseases. Given concerns over the potential toxicity from protracted use of cyclooxygenase inhibitors in the elderly, attention is now focused on blocking PGE2 signaling that is mediated by interactions with four distinct G protein-coupled receptors, EP1-4, which are differentially expressed on neuronal and glial cells throughout the central nervous system. EP1 activation has been shown to mediate Ca2+-dependent neurotoxicity in ischemic injury. EP2 activation has been shown to mediate microglial-induced paracrine neurotoxicity as well as suppress microglia internalization of aggregated neurotoxic peptides. Animal models support the potential efficacy of targeting specific EP receptor subtypes in Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, and ischemic stroke. However promising these preclinical studies are, they have yet to be followed by clinical trials targeting any EP receptor in neurologic diseases.
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