Caenorhabditis Elegans Models of Parkinson's Disease. A Robust Genetic System to Identify and Characterize Endogenous and Environmental Components Involved in Dopamine Neuron Degeneration

Richard Nass, Raja S. Settivari

Research output: Chapter in Book/Report/Conference proceedingChapter

5 Scopus citations

Abstract

This chapter presents a robust genetic system to identify and characterize endogenous and environmental components involved in dopamine neuron degeneration for the Caenorhabditis elegans (C. elegans) models of Parkinson's disease (PD). C. elegans is a powerful genetic model system for exploring the molecular mechanisms of neuronal function and disease. One of the most significant advantages of C. elegans is the ease of generating genetic knockdown or deletion mutants to identify gene function. C. elegans is sensitive to the mitochondria complex I inhibitor rotenone, the insecticide that has been weakly associated with the propensity to develop PD. It is found that of the genes identified to date that have been associated with PD, only α-synuclein does not have a clear ortholog in C. elegans. C. elegans overexpression of human α-synuclein may also increase overall fitness. It is suggested in vertebrates α-synuclein may also function as a chaperone and to protect against proapoptotic stimuli, and C. elegans could be a useful genetic model to begin to identify the molecular components involved in the α-synuclein neuroprotection.

Original languageEnglish (US)
Title of host publicationParkinson's Disease
PublisherElsevier Inc.
Pages347-360
Number of pages14
ISBN (Print)9780123740281
DOIs
StatePublished - Dec 1 2008

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ASJC Scopus subject areas

  • Neuroscience (miscellaneous)
  • Clinical Neurology
  • Psychiatry and Mental health

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