Caspase-3 Apoptotic Signaling Following Injury to the Central Nervous System
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Joe E. Springer
Abstract
Apoptotic cell death is a fundamental and highly regulated biological process in which a cell is instructed to participate actively in its own demise. This process of cellular suicide is activated by developmental and environmental cues and normally plays an essential role in eliminating superfluous, damaged, and senescent cells of many tissue types. In recent years, a number of experimental studies have provided evidence of widespread neuronal and glial apoptosis following injury to the central nervous system (CNS). These studies indicate that injury-induced apoptosis can be detected from hours to days following injury and may contribute to neurological dysfunction. Given these findings, understanding the biochemical signaling events controlling apoptosis is a first step towards developing therapeutic agents which would target this cell death process. This review will focus on the molecular cell death pathways responsible for generating the apoptotic phenotype, summarize what is currently known about apoptotic signals activated in the injured CNS, and what potential strategies might be pursued to reduce this cell death process as a means to promote functional recovery.
Copyright © 2001 by Walter de Gruyter GmbH & Co. KG
Articles in the same Issue
- IFCC/ Beckman Coulter Inc. Conference Frontiers in Molecular Basis of Diseases: Cell Biology of Neuronal Dysfunction, Paris, October 12-13, 2000
- Distribution of Cellular Prion Protein in Normal Human Cerebral Cortex – Does It Have Relevance to Creutzfeldt-Jakob Disease?
- Caspase-3 Apoptotic Signaling Following Injury to the Central Nervous System
- Parkinsons Disease and other α-Synucleinopathies
- Aggregation-Dependent Interaction of the Alzheimers β-Amyloid and Microglia
- β-Amyloid-Induced Cytotoxicity, Peroxide Generation and Blockade of Glutamate Uptake in Cultured Astrocytes
- Protein S-100B: A Serum Marker for Ischemic and Infectious Injury of Cerebral Tissue
- Reporting Cerebrospinal Fluid Data: Knowledge Base and Interpretation Software
- The Intrathecal Humoral Immune Response: Laboratory Analysis and Clinical Relevance
- Source of Endothelin-1 in Subarachnoid Hemorraghe
- Polymorphism of Apoprotein E (APOE), Methylenetetrahydrofolate Reductase (MTHFR) and Paraoxonase (PON1) Genes in Patients with Cerebrovascular Disease
- Neurotrophic Factor Therapy – Prospects and Problems
- Cell Therapy and Transplantation in Parkinsons Disease
- Matrix Metalloproteinases: Potential Therapeutic Target in Spinal Cord Injury
Articles in the same Issue
- IFCC/ Beckman Coulter Inc. Conference Frontiers in Molecular Basis of Diseases: Cell Biology of Neuronal Dysfunction, Paris, October 12-13, 2000
- Distribution of Cellular Prion Protein in Normal Human Cerebral Cortex – Does It Have Relevance to Creutzfeldt-Jakob Disease?
- Caspase-3 Apoptotic Signaling Following Injury to the Central Nervous System
- Parkinsons Disease and other α-Synucleinopathies
- Aggregation-Dependent Interaction of the Alzheimers β-Amyloid and Microglia
- β-Amyloid-Induced Cytotoxicity, Peroxide Generation and Blockade of Glutamate Uptake in Cultured Astrocytes
- Protein S-100B: A Serum Marker for Ischemic and Infectious Injury of Cerebral Tissue
- Reporting Cerebrospinal Fluid Data: Knowledge Base and Interpretation Software
- The Intrathecal Humoral Immune Response: Laboratory Analysis and Clinical Relevance
- Source of Endothelin-1 in Subarachnoid Hemorraghe
- Polymorphism of Apoprotein E (APOE), Methylenetetrahydrofolate Reductase (MTHFR) and Paraoxonase (PON1) Genes in Patients with Cerebrovascular Disease
- Neurotrophic Factor Therapy – Prospects and Problems
- Cell Therapy and Transplantation in Parkinsons Disease
- Matrix Metalloproteinases: Potential Therapeutic Target in Spinal Cord Injury
