Journal
NEUROCHEMICAL RESEARCH
Volume 29, Issue 9, Pages 1731-1737Publisher
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1023/B:NERE.0000035809.70905.8a
Keywords
Alzheimer's disease; COX-1; COX-2; COX-3; hippocampus; human neural cells; intron structure; NSAIDs
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Funding
- NIA NIH HHS [AG18031] Funding Source: Medline
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The cyclooxygenase ( COX) superfamily of prostaglandin synthase genes encode a constitutively expressed COX-1, an inducible, highly regulated COX-2, and a COX-3 isoform whose RNA is derived through the retention of a highly structured, G + C-rich intron 1 of the COX-1 gene. As generators of oxygen radicals, lipid mediators, and the pharmacological targets of nonsteroidal anti-inflammatory drugs ( NSAIDs), COX enzymes potentiate inflammatory neuropathology in Alzheimer's disease ( AD) brain. Because COX-2 is elevated in AD and COX-3 is enriched in the mammalian CNS, these studies were undertaken to examine the expression of COX-3 in AD and in [IL-1beta + Abeta42]-triggered human neural (HN) cells in primary culture. The results indicate that while COX-2 remains a major player in propagating inflammation in AD and in stressed HN cells, COX-3 may play ancillary roles in membrane-based COX signaling or when basal levels of COX-1 or COX-2 expression persist.
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