The etiopathogenesis of Parkinson disease and suggestions for future research. Part II

Irene Litvan, Marie Francoise Chesselet, Thomas Gasser, Donato A. Di Monte, Davis Parker, Theo Hagg, John Hardy, Peter Jenner, Richard H. Myers, Donald Price, Mark Hallett, William J. Langston, Anthony E. Lang, Glenda Halliday, Walter Rocca, Charles Duyckaerts, Dennis W. Dickson, Yoav Ben-Shlomo, Christopher G. Goetz, Eldad Melamed

Research output: Contribution to journalReview articlepeer-review


We are at a critical juncture in our knowledge of the etiology and pathogenesis of Parkinson disease (PD). It is clear that PD is not a single entity simply resulting from a dopaminergic deficit; rather it is most likely caused by a combination of genetic and environmental factors. Although there is extensive new information on the etiology and pathogenesis of PD, which may advance its treatment, new syntheses of this information are needed. The second part of this two-part, state-of-the-art review by leaders in PD research critically examines the research field to identify areas for which new knowledge and ideas might be helpful for treatment purposes. Topics reviewed in Part II are genetics, animal models, and oxidative stress.

Original languageEnglish
Pages (from-to)329-336
Number of pages8
JournalJournal of Neuropathology and Experimental Neurology
Issue number5
StatePublished - May 2007
Externally publishedYes


  • Lewy bodies
  • Parkinson disease
  • Synucleinopathies


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