, Volume 1, Issue 1, pp 139–154

Neurodegeneration and neuroprotection in Parkinson disease


DOI: 10.1602/neurorx.1.1.139

Cite this article as:
Fahn, S. & Sulzer, D. Neurotherapeutics (2004) 1: 139. doi:10.1602/neurorx.1.1.139


Many of the motoric features that define Parkinson disease (PD) result primarily from the loss of the neuromelanin (NM)-containing dopamine (DA) neurons of the substantia nigra (SN), and to a lesser extent, other mostly catecholaminergic neurons, and are associated with cytoplasmic “Lewy body” inclusions in some of the surviving neurons. While there are uncommon instances of familial PD, and rare instances of known genetic causes, the etiology of the vast majority of PD cases remains unknown (i.e., idiopathic). Here we outline genetic and environmental findings related to PD epidemiology, suggestions that aberrant protein degradation may play a role in disease pathogenesis, and pathogenetic mechanisms including oxidative stress due to DA oxidation that could underlie the selectivity of neurodegeneration. We then outline potential approaches to neuroprotection for PD that are derived from current notions on disease pathogenesis.

Key Words

PARK genes alpha-synuclein Parkin gene ubiquitin pathway 
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Copyright information

© The American Society for Experimental NeuroTherapeutics, Inc 2004

Authors and Affiliations

  1. 1.Department of NeurologyColumbia UniversityNew York
  2. 2.Neurological InstituteNew York

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