Cyclooxygenase-3 gene expression in alzheimer hippocampus and in stressed human neural cells

Jian Guo Cui, Hitoshi Kuroda, N. Vishvanath Chandrasekharan, Ricardo Palacios Pelaez, Daniel L. Simmons, Nicolas G. Bazan, Walter J. Lukiw

Research output: Contribution to journalArticlepeer-review

58 Scopus citations


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-1β 1 Aβ42]-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.

Original languageEnglish (US)
Pages (from-to)1731-1737
Number of pages7
JournalNeurochemical Research
Issue number9
StatePublished - Sep 2004


  • Alzheimer's disease
  • COX-1
  • COX-2
  • COX-3
  • hippocampus
  • human neural cells
  • intron structure
  • NSAIDs

ASJC Scopus subject areas

  • Neuroscience(all)
  • Biochemistry


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