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Part 1: Protein Aggregates

Benjamin Wolozin, MD, PhD; Christian Behl, PhD

Arch Neurol. 2000;57:793-796.

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

INTRODUCTION

Despite a vast array of causes of neurodegenerative diseases, research has identified common pathways through which the neurodegeneration proceeds. Part 1 of this neurological review article will address a confluence of research suggesting that neurodegeneration is often linked with the accumulation of insoluble protein aggregates; part 2, the mechanisms through which neurodegeneration occurs—apoptosis, necrosis, and excitotoxicity. Along with the common mechanisms for inducing neurodegeneration, we will also review common defense mechanisms that protect against toxic insults. Each of these pathways offers potential targets for pharmaceutical intervention.

ACCUMULATION OF PROTEIN AGGREGATES AS A PRIMARY DISEASE-INITIATING EVENT

One of the striking findings of neurodegeneration research is the observation that most of the proteins implicated in disease have a strong propensity to aggregate. For instance, neuritic senile plaques and neurofibrillary tangles are the hallmarks of Alzheimer disease (AD), Lewy bodies accumulate in Parkinson disease, and Pick bodies are prevalent in Pick disease. Even in diseases . . . [Full Text of this Article]

MECHANISMS OF AGGREGATION: INSIGHTS FROM -AMYLOID (A)

OTHER PROTEIN AGGREGATES

THE IMPLICATIONS OF AGGREGATION FOR MOLECULAR GENETICS

TRIGGERS OF NEURODEGENERATION AND KNOWN MECHANISMS OF NERVE CELL DEATH

THERAPEUTIC APPROACHES TO INHIBITING THE ACCUMULATION OF AGGREGATES

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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