APOPTOSIS: A PRACTICAL APPROACH
1 INTRODUCTION PART I CASPASE-INDEPENDENT PROGRAMMED CELL DEATH: GENERAL CONSIDERATIONS 2 CASPASE-INDEPENDENT CELL DEATH MECHANISMS IN SIMPLE ANIMAL MODELS 3 PROGRAMMED NECROSIS: A “NEW” CELL DEATH OUTCOME FOR INJURED ADULT NEURONS? 4 AGE-DEPENDENCE OF NEURONAL APOPTOSIS AND OF CASPASE ACTIVATION 5 EXCITOTOXIC PROGRAMMED CELL DEATH INVOLVES CASPASE-INDEPENDENT MECHANISMS PART II FOCAL CEREBRAL ISCHEMIA 6 SIGNIFICANT ROLE OF APOPTOSIS-INDUCING FACTOR (AIF) FOR BRAIN DAMAGE FOLLOWING FOCAL CEREBRAL ISCHEMIA 7 THE ROLE OF POLY(ADP-RIBOSE) POLYMERASE-1 (PARP-1) ACTIVATION IN FOCAL CEREBRAL ISCHEMIA CONTENTS PART III TRANSIENT GLOBAL ISCHEMIA 8 TRANSIENT GLOBAL CEREBRAL ISCHEMIA PRODUCES MORPHOLOGICALLY NECROTIC, NOT APOPTOTIC NEURONS 9 APOPTOSIS-INDUCING FACTOR TRANSLOCATION TO NUCLEI AFTER TRANSIENT GLOBAL ISCHEMIA 10 ROLE OF µ-CALPAIN I AND LYSOSOMAL CATHEPSINS IN HIPPOCAMPAL NEURONAL NECROSIS AFTER TRANSIENT GLOBAL ISCHEMIA IN PRIMATES PART IV TRAUMATIC CENTRAL NERVOUS SYSTEM (CNS) INJURY 11 MITOCHONDRIAL DAMAGE IN TRAUMATIC CNS INJURY 12 PROGRAMMED NEURONAL CELL DEATH MECHANISMS IN CNS INJURY PART V HYPOGLYCEMIC NEURONAL DEATH 13 HYPOGLYCEMIC BRAIN DAMAGE 14 HYPOGLYCEMIC NEURONAL DEATH PART VI SEIZURE-INDUCED NEURONAL DEATH 15 TUMOR SUPPRESSOR P53: A MULTIFUNCTIONAL PROTEIN IMPLICATED IN SEIZURE-INDUCED NEURONAL CELL DEATH 16 DNA DAMAGE AND REPAIR IN THE BRAIN: IMPLICATIONS FOR SEIZURE- INDUCED NEURONAL INJURY, ENDANGERMENT, AND NEUROPROTECTION 17 ACTIVATION OF CASPASE-INDEPENDENT PROGRAMMED PATHWAYS IN SEIZURE-INDUCED NEURONAL NECROSIS CONCLUDING REMARKS