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Oxidative Medicine and Cellular Longevity
Volume 2017 (2017), Article ID 7371403, 10 pages
Research Article

Plasma DNA Mediate Autonomic Dysfunctions and White Matter Injuries in Patients with Parkinson’s Disease

1Department of Diagnostic Radiology, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung, Taiwan
2Chang Gung University College of Medicine, Kaohsiung, Taiwan
3Department of Neurology, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung, Taiwan
4Graduate Institute of Medical Mechatronics, Chang Gung University, Taoyuan, Taiwan
5Department of Neurology, Chang Gung Memorial Hospital, Linkou, Taoyuan, Taiwan
6Department of Medicine, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung, Taiwan

Correspondence should be addressed to Wei-Che Lin

Received 1 September 2016; Revised 8 November 2016; Accepted 19 December 2016; Published 23 January 2017

Academic Editor: James Duce

Copyright © 2017 Meng-Hsiang Chen et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Background. Cardiovascular autonomic dysfunction is well known in Parkinson’s disease (PD) presentation and it produces hypoperfusion of vital organs. The association between cardiovascular autonomic dysfunction and oxidative stress was examined in previous animal models. Oxidative stress and neuroinflammation were thought to have roles in PD pathogenesis. Owing to the relative low intrinsic antioxidative properties, brain white matter (WM) is vulnerable to the oxidative stress. This study is conducted to examine possible relationships by using a hypothesis-driven mediation model. Methods. Twenty-nine patients with PD and 26 healthy controls participated in this study, with complete examinations of cardiac autonomic parameters, plasma DNA level, and WM integrity. A single-level three-variable mediation model was used to investigate the possible relationships. Results. The elevated serum oxidative stress biomarkers include plasma nuclear DNA and mitochondrial DNA, and poorer cardiac autonomic parameters and multiple regional microstructural WM changes are demonstrated. Further mediation analysis shows that plasma nuclear DNA served as the mediators between poorer baroreflex sensitivity and mean diffusivity changes in cingulum. Conclusions. These results provide a possible pathophysiology for how the poor baroreflex sensitivity and higher oxidative stress adversely impacted the WM integrity. This model could provide us with a piece of the puzzle of the entire PD pathogenesis.