Molecular pathophysiology of Parkinson's disease

Darren J. Moore, Andrew B. West, Valina Dawson, Ted M Dawson

Research output: Contribution to journalArticle

Abstract

Parkinson's disease (PD) is a progressive neurodegenerative movement disorder that results primarily from the death of dopaminergic neurons in the substantia nigra. Although the etiology of PD is incompletely understood, the recent discovery of genes associated with rare monogenic forms of the disease, together with earlier studies and new experimental animal models, has provided important and novel insight into the molecular pathways involved in disease pathogenesis. Increasing evidence indicates that deficits in mitochondrial function, oxidative and nitrosative stress, the accumulation of aberrant or misfolded proteins, and ubiquitin-proteasome system dysfunction may represent the principal molecular pathways or events that commonly underlie the pathogenesis of sporadic and familial forms of PD.

Original languageEnglish (US)
Pages (from-to)57-87
Number of pages31
JournalAnnual Review of Neuroscience
Volume28
DOIs
StatePublished - 2005

    Fingerprint

Keywords

  • α-synuclein
  • Mitochondrial complex-I
  • Oxidative stress
  • Parkin
  • Ubiquitin-proteasome system

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this