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  Vol. 57 No. 6, June 2000 TABLE OF CONTENTS
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Mechanisms of Neurodegenerative Disorders

Part 2: Control of Cell Death

Benjamin Wolozin, MD, PhD; Christian Behl, PhD

Arch Neurol. 2000;57:801-804.

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

INTRODUCTION

Recent research into mechanisms of neurodegeneration in Alzheimer disease (AD), Parkinson disease, and other neurodegenerative disorders has lead to a dramatic increase in our understanding of the mechanisms of cell death and neuroprotection. Apoptosis is an active form of cell death that is carried out by proteins that are designed to kill the cell. Necrosis tends to occur as a by-product of excessive oxidative stress, which can be induced by agents such as {beta}-amyloid, or excessive calcium influx induced by agents such as glutamate. The neuron also has strong homeostatic mechanisms that can delay or prevent activation of apoptosis and necrosis. The balance between neurotoxic and neuroprotective mechanisms determines whether a neuron lives or dies.


CELL DEATH AS NATURALLY OCCURRING MECHANISM IN THE DEVELOPMENT OF THE NERVOUS SYSTEM AND DURING NEURODEGENERATIVE EVENTS

Much of our knowledge of cell death comes from studies of physiological "programmed cell death." The term programmed cell death refers to the physiological suicide program that is . . . [Full Text of this Article]

CASPASES AS EXECUTORS OF CELL DEATH

APOPTOSIS IN NEURODEGENERATION

PRESENILINS AND APOPTOSIS

NECROSIS IN NEURODEGENERATION

NEUROPROTECTION: EXOGENOUS NEUROPROTECTION AND INTRACELLULAR NEUROPROTECTION—BASIC RESEARCH AND CLINICAL PERSPECTIVES

OUTLOOK

From the Department of Pharmacology, Loyola University Medical Center, Maywood, Ill (Dr Wolozin); and the Max-Planck-Institute of Psychiatry, Munich, Germany (Dr Behl).


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