Mechanisms of Neurodegenerative Disorders
Part 1: Protein Aggregates
Benjamin Wolozin, MD, PhD;
Christian Behl, PhD
Arch Neurol. 2000;57:793-796.
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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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