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  Vol. 57 No. 9, September 2000 TABLE OF CONTENTS
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  Basic Science Seminars in Neurology
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Role of Caspase 1 in Neurologic Disease

Robert M. Friedlander, MD, MA

Arch Neurol. 2000;57:1273-1276.

Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

INTRODUCTION

In recent years substantial advances have taken place in understanding the mechanistic pathways mediating neuronal cell death in a variety of neurologic diseases. Since the central nervous system (CNS) has little, if any, power of functional neuronal regeneration, prevention of neuronal cell death is an important target of modern neurotherapeutics. A detailed understanding of the mechanisms mediating neuronal cell death is required to effectively slow the progression of neurologic diseases featuring apoptosis. Increasing evidence demonstrates that blocking cell death pathways in cells otherwise fated to die (ie, following stroke, trauma, or in neurodegenerative diseases) improves neurologic outcome.1-7

Broadly, cells can die by 1 of 2 mechanisms: necrosis or apoptosis. Necrotic cell death is a more passive form of cell death, where the stimulus itself alters cell homeostasis resulting in its death. On the other hand, apoptosis (also known as programmed cell death) is a more . . . [Full Text of this Article]

ACUTE CELL DEATH DISEASES

CHRONIC CELL DEATH DISEASES

Amyotrophic Lateral Sclerosis

Huntington Disease

CONCLUSIONS

From the Neuroapoptosis Laboratory, Neurosurgical Service, Department of Surgery, Brigham and Women's Hospital, Harvard Medical School, Boston, Mass.


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