scholarly journals The Potential Effects of Oxidative Stress-Related Plasma Abnormal Protein Aggregate Levels on Brain Volume and Its Neuropsychiatric Consequences in Parkinson’s Disease

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Pei-Chin Chen ◽  
Chiun-Chieh Yu ◽  
Yueh-Sheng Chen ◽  
Cheng-Hsien Lu ◽  
Shan-Ho Chan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Cognitive Decline ◽  
Brain Volume ◽  
Mediation Model ◽  
Protein Aggregate ◽  
Abnormal Protein ◽  
Regional Brain ◽  
Regional Brain Volume

Background. Oxidative stress has been implicated in the pathogenesis of many diseases, including Parkinson’s disease. Large protein aggregates may be produced after the breakdown of the proteostasis network due to overt oxidative stress. Meanwhile, brain volume loss and neuropsychiatric deficits are common comorbidities in Parkinson’s disease patients. In this study, we applied a mediation model to determine the potential influences of oxidative stress-related plasma abnormal protein aggregate levels on brain volume and neuropsychiatric consequences in Parkinson’s disease. Method. 31 patients with PD and 24 healthy controls participated in this study. The PD patients were further grouped according to the presentation of cognitive decline or not. All participants received complete examinations to determine plasma abnormal protein aggregates levels, brain volume, and neuropsychiatric performance. The results were collected and analyzed in a single-level three-variable mediation model. Results. Patients with PD cognitive decline exhibited higher plasma NfL levels, decreased regional brain volume, and poor neuropsychiatric subtest results compared with PD patients with normal cognition, with several correlations among these clinical presentations. The mediation model showed that the superior temporal gyrus completely mediated the effects of elevated plasma NfL levels due to the poor psychiatric performance of picture completion and digit span. Conclusion. This study provides insight into the effects of oxidative stress-related plasma abnormal protein aggregate levels on regional brain volume and neuropsychiatric consequences in Parkinson’s disease patients.

scholarly journals Etiology of Parkinson's Disease

2003 ◽  
Vol 30 (S1) ◽  
pp. S10-S18 ◽  
Author(s):  
Zhigao Huang ◽  
Raúl de la Fuente-Fernández ◽  
A. Jon Stoessl
Keyword(s):  
Oxidative Stress ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Environmental Factors ◽  
Neurodegenerative Disorders ◽  
Caffeine Intake ◽  
Genetic Mutations ◽  
Abnormal Protein ◽  
Relative Contribution ◽  
Genetic And Environmental Factors

There is growing recognition that Parkinson's disease (PD) is likely to arise from the combined effects of genetic predisposition as well as largely unidentified environmental factors. The relative contribution of each varies from one individual to another. Even in situations where more than one family member is affected, the predominant influence may be environmental. Although responsible for only a small minority of cases of PD, recently identified genetic mutations have provided tremendous insights into the basis for neurodegeneration and have led to growing recognition of the importance of abnormal protein handling in Parkinson's as well as other neurodegenerative disorders. Abnormal protein handling may increase susceptibility to oxidative stress; conversely, numerous other factors, including oxidative stress and impaired mitochondrial function can lead to impaired protein degradation. A limited number of environmental factors are known to be toxic to the substantia nigra; in contrast, some factors such as caffeine intake and cigarette smoking may protect against the development of PD, although the mechanisms are not established. We review the various genetic and environmental factors thought to be involved in PD, as well as the mechanisms that contribute to selective nigral cell death.

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

2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
Meng-Hsiang Chen ◽  
Pei-Chin Chen ◽  
Cheng-Hsien Lu ◽  
Hsiu-Ling Chen ◽  
Yi-Ping Chao ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
White Matter ◽  
Autonomic Dysfunction ◽  
Baroreflex Sensitivity ◽  
Nuclear Dna ◽  
Mediation Model ◽  
Plasma Dna ◽  
Cardiovascular Autonomic Dysfunction

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.

scholarly journals Pretreatment brain volumes can affect the effectiveness of deep brain stimulation in Parkinson's disease patients

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Younghee Yim ◽  
Sang Joon Kim ◽  
Seung Chai Jung ◽  
Ho Sung Kim ◽  
Choong Gon Choi ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Deep Brain Stimulation ◽  
Brain Stimulation ◽  
Brain Volume ◽  
Anterior Cingulate ◽  
Brain Volumes ◽  
Regional Brain ◽  
Motor Improvement ◽  
Deep Brain

AbstractWe aimed to assess whether brain volumes may affect the results of deep brain stimulation (DBS) in patients with Parkinson’s disease (PD). Eighty-one consecutive patients with PD (male:female 40:41), treated with DBS between June 2012 and December 2017, were enrolled. Total and regional brain volumes were measured using automated brain volumetry (NeuroQuant). The Unified Parkinson Disease Rating Scale motor score quotient was used to assess changes in clinical outcome and compare the preoperative regional brain volume in patients categorized into the higher motor improvement and lower motor improvement groups based on changes in the postoperative scores. The study groups showed significant volume differences in multiple brain areas. In the higher motor improvement group, the anterior cingulate and right thalamus showed high volumes after false discovery rate (FDR) correction. In the lower motor improvement group, the left caudate, paracentral, right primary sensory and left primary motor cortex showed high volume, but no area showed high volumes after FDR correction. Our data suggest that the effectiveness of DBS in patients with PD may be affected by decreased brain volume in different areas, including the cingulate gyrus and thalamus. Preoperative volumetry could help predict outcomes in patients with PD undergoing DBS.

Mitochondria as an Easy Target to Oxidative Stress Events in Parkinson's Disease

2012 ◽  
Vol 11 (4) ◽  
pp. 430-438 ◽  
Author(s):  
Marcella Reale ◽  
Mirko Pesce ◽  
Medha Priyadarshini ◽  
Mohammad A Kamal ◽  
Antonia Patruno
Keyword(s):  
Oxidative Stress ◽  
Parkinson’S Disease ◽  
Parkinson's Disease

scholarly journals The Contribution of Microglia to Neuroinflammation in Parkinson’s Disease

2021 ◽  
Vol 22 (9) ◽  
pp. 4676
Author(s):  
Katja Badanjak ◽  
Sonja Fixemer ◽  
Semra Smajić ◽  
Alexander Skupin ◽  
Anne Grünewald
Keyword(s):  
Oxidative Stress ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Inflammatory Cytokine ◽  
Population Ageing ◽  
Future Research ◽  
Cytokine Release ◽  
Vicious Cycle ◽  
Inflammatory Processes ◽  
Great Evidence

With the world’s population ageing, the incidence of Parkinson’s disease (PD) is on the rise. In recent years, inflammatory processes have emerged as prominent contributors to the pathology of PD. There is great evidence that microglia have a significant neuroprotective role, and that impaired and over activated microglial phenotypes are present in brains of PD patients. Thereby, PD progression is potentially driven by a vicious cycle between dying neurons and microglia through the instigation of oxidative stress, mitophagy and autophagy dysfunctions, a-synuclein accumulation, and pro-inflammatory cytokine release. Hence, investigating the involvement of microglia is of great importance for future research and treatment of PD. The purpose of this review is to highlight recent findings concerning the microglia-neuronal interplay in PD with a focus on human postmortem immunohistochemistry and single-cell studies, their relation to animal and iPSC-derived models, newly emerging technologies, and the resulting potential of new anti-inflammatory therapies for PD.

scholarly journals Modifiable comorbidities associated with cognitive decline in Parkinson's Disease

2020 ◽  
Author(s):  
Emily Forbes ◽  
Thomas F. Tropea ◽  
Sneha Mantri ◽  
Sharon X. Xie ◽  
James F. Morley
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Cognitive Decline
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