The central nervous system (CNS) is a major dose-limiting organ in clinical …

• Abstract
• Introduction
• Specific cell types in the central nervous system and their function
• Clinical radiation therapy
• Histopathologic changes
• Early gene induction
• Apoptosis
• Inhibition of neurogenesis
• Hypoxia, barrier disruption, and necrosis of the white matter
• ICAM-1
• Cell replacement
• Reducing apoptotic cell death
• Reducing secondary cell death
• Conclusion
• References
• Figure

Biology Articles » Biophysics » Medical Biophysics » Mechanisms of radiation injury to the central nervous system: implications for neuroprotection » Introduction

Introduction

- Mechanisms of radiation injury to the central nervous system: implications for neuroprotection

Radiation therapy (XRT) is a major cancer treatment modality. About 40% of all cancer patients receive XRT during their illness either for cure or for local control or symptomatic palliation (1). The effectiveness of XRT is, to a large extent, limited by the potential for normal tissue injury. Radiation injury of the central nervous system (CNS), consisting of the brain and spinal cord, has devastating clinical consequences. Because of its anatomic location, the CNS is not only dose-limiting in the treatment of CNS tumors, but also in the treatment of head and neck, thoracic, and upper abdominal malignancies. The underlying mechanisms of this injury remain unclear; however, there is an increasing body of data indicating that the response of the CNS after XRT is a continuous, dynamic, and interacting process (2). It is now recognized that clonogenic cell death is not the only mode of cell death in the CNS after XRT (3–8). Certain glial, neuronal, and endothelial cells in the CNS also undergo apoptosis soon after XRT. Furthermore, there is a component of secondary injury and cell death that is mediated by microenvironmental alterations such as hypoxia/ischemia and inflammation (9–13). This review addresses these potentially reversible components of the injury response and their implications on neuroprotective interventions.