α-Synuclein nonhuman primate models of Parkinson’s disease

David J. Marmion, Jeffrey H. Kordower

Research output: Contribution to journalReview articlepeer-review

16 Scopus citations

Abstract

Proper understanding of the mechanism(s) by which α-synuclein misfolds and propagates may hold the key to unraveling the complex pathophysiology of Parkinson’s disease. A more complete understanding of the disease itself, as well as establishing animal models that fully recapitulate pathological and functional disease progression, are needed to develop treatments that will delay, halt or reverse the disease course. Traditional neurotoxin-based animal models fail to mimic crucial aspects of Parkinson’s and thus are not relevant for the study of neuroprotection and disease-modifying therapies. Therefore, a new era of animal models centered on α-synuclein has emerged with the utility of nonhuman primates in these studies beginning to become important. Indeed, disease modeling in nonhuman primates offers a more similar anatomical and genetic background to humans, and the ability to assess complex behavioral impairments that are difficult to test in rodents. Furthermore, results obtained from monkey studies translate better to applications in humans. In this review, we highlight the importance of α-synuclein in Parkinson’s disease and discuss the development of α-synuclein based nonhuman primate models.

Original languageEnglish (US)
Pages (from-to)385-400
Number of pages16
JournalJournal of Neural Transmission
Volume125
Issue number3
DOIs
StatePublished - Mar 1 2018
Externally publishedYes

Keywords

  • Alpha-synuclein
  • Animal models
  • Nonhuman primate
  • Parkinson's disease

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology
  • Psychiatry and Mental health
  • Biological Psychiatry

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