Molecular pathogenesis of Parkinson disease

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Abstract

Parkinson disease (PD), the most common neurodegenerative movement disorder, is characterized by an extensive and progressive loss of dopaminergic neurons in the substantia nigra pars compacta. One of the pathological hallmarks of PD is the presence of Lewy bodies, intracellular inclusions of aggregated α-synuclein. Although the cause and pathogenesis of selective loss of dopamine neurons and the accumulation of α-synuclein in PD remain elusive, growing lines of evidence from environmental risk factors and early-onset genetics point to a convergence between energy metabolism and the disposal of damaged proteins in the development of PD. These findings suggest that impairments in mitochondrial and ubiquitin-proteasome system function can significantly contribute to the pathogenesis of PD. This review will summarize recent insights gained from genetic and environmental studies of PD that underscore this association.

Original languageEnglish (US)
Pages (from-to)353-357
Number of pages5
JournalArchives of neurology
Volume62
Issue number3
DOIs
StatePublished - Mar 1 2005

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ASJC Scopus subject areas

  • Arts and Humanities (miscellaneous)
  • Clinical Neurology

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