1. ^*Division of Clinical Neuroscience, Faculty of Medicine, University of Glasgow, Glasgow, United Kingdom
2. ^†Department of Neurology and Center for the Study of Nervous System Injury, Washington University School of Medicine, St. Louis, Missouri, U.S.A.

Correspondence: Deborah Dewar, Division of Clinical Neuroscience, University of Glasgow, Wellcome Surgical Institute, Garscube Estate, Bearsden road, Glasgow G61 1QH, U.K. E-mail: d.dewar@udcf.gla.ac.uk

Received 27 November 2002; Accepted 6 December 2002.

Abstract

Oligodendrocytes, myelin-forming glial cells of the central nervous system, are vulnerable to damage in a variety of neurologic diseases. Much is known of primary myelin injury, which occurs in settings of genetic dysmyelination or demyelinating disease. There is growing awareness that oligodendrocytes are also targets of injury in acute ischemia. Recognition of oligodendrocyte damage in animal models of ischemia requires attention to their distinct histologic features or use of specific immunocytochemical markers. Like neurons, oligodendrocytes are highly sensitive to injury by oxidative stress, excitatory amino acids, trophic factor deprivation, and activation of apoptotic pathways. Understanding mechanisms of oligodendrocyte death may suggest new therapeutic strategies to preserve or restore white matter function and structure after ischemic insults.