» Articles » PMID: 28520211

Aging and Parkinson's Disease: Different Sides of the Same Coin?

Overview
Journal Mov Disord
Date 2017 May 19
PMID 28520211
Citations 116
Authors
Affiliations
Soon will be listed here.
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. © 2017 The Authors. Movement Disorders published by Wiley Periodicals, Inc. on behalf of International Parkinson and Movement Disorder Society.

Citing Articles

Longitudinal multi-omics in alpha-synuclein Drosophila model discriminates disease- from age-associated pathologies in Parkinson's disease.

Moore J, Wu T, Dhindsa J, El Fadel O, Le A, Perez A NPJ Parkinsons Dis. 2025; 11(1):46.

PMID: 40069190 PMC: 11897226. DOI: 10.1038/s41531-025-00899-z.


Temporal Trends in Parkinson's Disease Related Mortality from 1999-2020: A National Analysis.

Sokhal B, Prasanna Kumar Menon S, Shepherd T, Muller S, Arora A, Mallen C NIHR Open Res. 2025; 4():50.

PMID: 39830305 PMC: 11739699. DOI: 10.3310/nihropenres.13623.1.


The centenarian blueprint: lessons in defying Parkinson's disease.

Bhidayasiri R, Aiba I, Nomoto M J Neural Transm (Vienna). 2024; 132(3):331-339.

PMID: 39729254 DOI: 10.1007/s00702-024-02875-y.


Assessing age-related changes in brain activity during isometric upper and lower limb force control tasks.

Bower A, Chung J, Burciu R Brain Struct Funct. 2024; 230(1):6.

PMID: 39688714 PMC: 11652581. DOI: 10.1007/s00429-024-02866-5.


Should We Consider Neurodegeneration by Itself or in a Triangulation with Neuroinflammation and Demyelination? The Example of Multiple Sclerosis and Beyond.

Perdaens O, van Pesch V Int J Mol Sci. 2024; 25(23.

PMID: 39684351 PMC: 11641818. DOI: 10.3390/ijms252312637.


References
1.
Durcan T, Fon E . The three 'P's of mitophagy: PARKIN, PINK1, and post-translational modifications. Genes Dev. 2015; 29(10):989-99. PMC: 4441056. DOI: 10.1101/gad.262758.115. View

2.
Chu Y, Dodiya H, Aebischer P, Olanow C, Kordower J . Alterations in lysosomal and proteasomal markers in Parkinson's disease: relationship to alpha-synuclein inclusions. Neurobiol Dis. 2009; 35(3):385-98. DOI: 10.1016/j.nbd.2009.05.023. View

3.
Stark A, Pakkenberg B . Histological changes of the dopaminergic nigrostriatal system in aging. Cell Tissue Res. 2004; 318(1):81-92. DOI: 10.1007/s00441-004-0972-9. View

4.
Chu Y, Le W, Kompoliti K, Jankovic J, Mufson E, Kordower J . Nurr1 in Parkinson's disease and related disorders. J Comp Neurol. 2005; 494(3):495-514. PMC: 2564615. DOI: 10.1002/cne.20828. View

5.
Kenyon C, Chang J, Gensch E, Rudner A, Tabtiang R . A C. elegans mutant that lives twice as long as wild type. Nature. 1993; 366(6454):461-4. DOI: 10.1038/366461a0. View