Molecular Pathways of Neurodegeneration in Parkinson's Disease

Research output: Contribution to journalReview articlepeer-review

Abstract

Parkinson's disease (PD) is a complex disorder with many different causes, yet they may intersect in common pathways, raising the possibility that neuroprotective agents may have broad applicability in the treatment of PD. Current evidence suggests that mitochondrial complex I inhibition may be the central cause of sporadic PD and that derangements in complex I cause α-synuclein aggregation, which contributes to the demise of dopamine neurons. Accumulation and aggregation of α-synuclein may further contribute to the death of dopamine neurons through impairments in protein handling and detoxification. Dysfunction of parkin (a ubiquitin E3 ligase) and DJ-1 could contribute to these deficits. Strategies aimed at restoring complex I activity, reducing oxidative stress and α-synuclein aggregation, and enhancing protein degradation may hold particular promise as powerful neuroprotective agents in the treatment of PD.

Original languageEnglish (US)
Pages (from-to)819-822
Number of pages4
JournalScience
Volume302
Issue number5646
DOIs
StatePublished - Oct 31 2003

ASJC Scopus subject areas

  • General

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