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Review : Apoptosis and Spinal Cord Injury

Department of Cell Biology, Neurobiology, and Anatomy (MSB, SLS, JCB) and Division of Neurosurgery (MSB) The Ohio State University College of Medicine and Public Health Columbus, Ohio

Sheri L. Shuman

Department of Cell Biology, Neurobiology, and Anatomy (MSB, SLS, JCB) and Division of Neurosurgery (MSB) The Ohio State University College of Medicine and Public Health Columbus, Ohio

Jacqueline C. Bresnahan

Department of Cell Biology, Neurobiology, and Anatomy (MSB, SLS, JCB) and Division of Neurosurgery (MSB) The Ohio State University College of Medicine and Public Health Columbus, Ohio

Apoptosis is the morphological counterpart of active, genetically programmed cell death and is important in development, immune function, and carcinogenesis. Recent data suggest that apoptosis may be important in neurodegenerative disorders, ischemic brain injury, and neurotrauma as well. Here we review very recent data from our laboratory and others that show that at least some of the pronounced secondary injury that follows spinal cord injury (SCI) may be caused by apoptosis and associated intracellular death pathways. Both neurons and glia seem to die by apoptosis; the response of oligodendrocytes in long tracts undergoing Wallerian degeneration is particularly long lived and may be responsible for chronic demyelination and some of the dysfunction in chronic SCI. These findings suggest that the therapeutic window for treatment of acute SCI may extend into the chronic phase. In addition, proliferation of ependymal cells occurs in concert with cell death, suggesting that both degeneration and repair may occur at the same time. Therapies aimed at altering the balance between these cellular events may be useful for future treatments of SCI. NEURO SCIENTIST 4:163-171, 1998

Key Words: KEY WORDS Apoptosis • Oligodendrocytes • Injury • Spinal cord • Axons

The Neuroscientist, Vol. 4, No. 3, 163-171 (1998)
DOI: 10.1177/107385849800400312


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