Controversies in Neurology
April 2003

Cyclooxygenases in Central Nervous System DiseasesA Special Role for Cyclooxygenase 2 in Neuronal Cell Death

Author Affiliations

From the Geriatric Research Educational and Clinical Center, Veterans Affairs Pittsburgh Health Care System (Dr Graham), and the Departments of Neurology (Dr Graham) and Pediatrics (Dr Hickey), University of Pittsburgh School of Medicine, Pittsburgh, Pa.




Copyright 2003 American Medical Association. All Rights Reserved. Applicable FARS/DFARS Restrictions Apply to Government Use.2003

Arch Neurol. 2003;60(4):628-630. doi:10.1001/archneur.60.4.628

IN THIS issue of the ARCHIVES, Schwab and Schluesener1 address the roles of cyclooxygenase 1 (COX-1) and cyclooxygenase 2 (COX-2) in central nervous system (CNS) diseases and injury. First, they argue that COX-1 activity in CNS diseases has been overlooked. They point out that COX-1, although it is a constitutively expressed enzyme, accumulates under pathophysiologic conditions of chronic injury. Specifically, COX-1 is expressed in the microglia and macrophages that accumulate during recovery from hypoxic-ischemic or traumatic brain injury. It is also expressed in microglia and macrophages in Alzheimer disease. Second, Schwab and Schluesener also point out that our understanding of inflammation has recently been complicated by evidence suggesting that an initial proinflammatory burst of prostaglandin production can be followed by prostaglandin-mediated anti-inflammatory (reparative) responses. Evidence that COX-2 can play a role in the resolution of inflammation and wound healing in non-CNS tissues raises the possibility that COX-2 may have an as yet uncharacterized delayed reparative effect in CNS injury. Thus, Schwab and Schluesener argue that the emphasis on COX-2 as a pathogenic factor in CNS injury is misplaced.

First Page Preview View Large
First page PDF preview
First page PDF preview