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Controversies in Neurology
April 2003

Similar Enzymes, Different Mechanisms: COX-1 and COX-2 Enzymes in Neurologic Disease

Author Affiliations

From the Department of Neurology, University of Pittsburgh, Pittsburgh, Pa.



Arch Neurol. 2003;60(4):632-633. doi:10.1001/archneur.60.4.632

DETERMINING THE pathological cascades that lead to clinically apparent neurologic disease requires knowledge of both the biochemical entities involved in these sequences and the time dimension in which they occur. Thus, inflammatory changes in the central nervous system have a characteristic course, but chronic inflammatory and neurodegenerative disorders may begin years before they manifest clinical symptoms. In the discussion this month, Drs Schwab and Schluesener propose that both variants of cyclooxygenase (COX) enzymes, COX-1 and COX-2, have roles to play by virtue of their temporal sequences in response to injury. Schwab and Schluesener argue that in our eagerness to determine the role of COX-2 in acute or subacute inflammatory or degenerative disorders in humans, we focus on it because it is a reactive gene product. A constitutively expressed enzyme, COX-1 has attracted less attention as an effector of neurologic disorders because it is constitutively expressed. Schwab and Schluesener make the point that both of these enzymes may have roles to play in neurologic disease and offer as a prime exhibit the slow increase and protracted presence of COX-1 elevation in certain central nervous system inflammatory disorders.

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