Journal
MOVEMENT DISORDERS
Volume 32, Issue 7, Pages 983-990Publisher
WILEY
DOI: 10.1002/mds.27037
Keywords
aging; Parkinson's disease; nonhuman primates; proteasome; lysosome; oxidative stress; microglia
Categories
Funding
- NINDS NIH HHS [R01 NS082730, R01 NS094460] Funding Source: Medline
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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. (C) 2017 The Authors. Movement Disorders published by Wiley Periodicals, Inc. on behalf of International Parkinson and Movement Disorder Society.
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