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NEUROLOGY 2006;66:S24-S36
© 2006 American Academy of Neurology

Neurology supplements are not peer-reviewed. Information contained in Neurology supplements represent the opinions of the authors and are not endorsed by nor do they reflect the views of the American Academy of Neurology, Editor-in-Chief, or Associate Editors of Neurology.

The pathogenesis of cell death in Parkinson's disease

Peter Jenner, PhD and C. Warren Olanow, MD, FRCPC

From the Neurodegenerative Diseases Research Centre, School of Health and Biomedical Sciences, King's College, London, United Kingdom (Dr. Jenner), and the Departments of Neurology and Neuroscience, Mount Sinai School of Medicine, New York, New York (Dr. Olanow).

Address correspondence and reprint requests to Dr. Peter Jenner, NDRC, School of Health and Biomedical Sciences, King's College, London SE1 1UL, UK; e-mail: peter.jenner{at}kcl.ac.uk

Concepts of pathogenesis in Parkinson's disease (PD) have been based on attempts to understand the mechanisms responsible for nigral dopaminergic cell death. Pathogenesis has been proposed to involve oxidative and nitrative stress, excitotoxicity, inflammation, mitochondrial dysfunction, and altered proteolysis. These processes are considered to form a complex cascade of interrelated events that lead to neuron death by way of apoptosis. However, current views on pathogenic mechanisms in PD may not be as exact as commonly proposed. Future concepts of pathogenesis in PD need to incorporate events leading to the destruction of non-dopaminergic nuclei and to distinguish between primary factors that are responsible for disease initiation and secondary factors that contribute to disease progression. Importantly, there is a need to determine whether PD is a single illness with a common pathogenesis or a group of related illnesses with different pathogenic mechanisms. This is an essential step to understanding pathogenesis and is critical to the development of comprehensive neuroprotective approaches to treatment.


Publication of this supplement was supported by an educational grant from Teva Neuroscience and Eisai, Inc.

Disclosure: PJ has received the following from the sponsor of this supplement: an honorarium for his participation in this project and personal honoraria during his career. The sponsor has provided CWO with personal honoraria (in excess of $10,000) during his professional career.




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