Aging and Parkinson's disease: Different sides of the same coin?

Timothy J. Collier, Nicholas M. Kanaan, Jeffrey H. Kordower

Research output: Contribution to journalReview articlepeer-review

94 Scopus citations

Abstract

Despite abundant epidemiological evidence in support of aging as the primary risk factor for PD, biological correlates of a connection have been elusive. In this article, we address the following question: does aging represent biology accurately characterized as pre-PD? We present evidence from our work on midbrain dopamine neurons of aging nonhuman primates that demonstrates that markers of known correlates of dopamine neuron degeneration in PD, including impaired proteasome/lysosome function, oxidative/nitrative damage, and inflammation, all increase with advancing age and are exaggerated in the ventral tier substantia nigra dopamine neurons most vulnerable to degeneration in PD. Our findings support the view that aging-related changes in the dopamine system approach the biological threshold for parkinsonism, actively producing a vulnerable pre-parkinsonian state.

Original languageEnglish (US)
Pages (from-to)983-990
Number of pages8
JournalMovement Disorders
Volume32
Issue number7
DOIs
StatePublished - Jul 2017
Externally publishedYes

Keywords

  • aging
  • lysosome
  • microglia
  • nonhuman primates
  • oxidative stress
  • Parkinson's disease
  • proteasome

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology

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