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Mitochondrial Dysfunction and Oxidative Stress in Parkinson’s Disease

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".

Deadline for manuscript submissions: 31 July 2024 | Viewed by 1743

Special Issue Editor

Special Issue Information

Dear Colleagues,

Parkinson’s disease (PD) is one of the most common progressive neurodegenerative disorders of which the aetiology is still largely unknown. Although, mitochondrial dysfunction and oxidative stress (OS) are thought to be important pathophysiological factors in the disease progression.

Mitochondrial dysfunction centred at complex I of the mitochondrial respiratory chain (MRC) has been well documented in the substantia nigra of patients with PD; although the cause of this impairment has yet to be fully elucidated, it may be the result of OS-induced oxidative damage to the MRC and mitochondrial DNA. Interestingly, mutations in several genes associated with the familial forms of PD can also impact mitochondrial function, although whether this results in a direct impairment of MRC enzyme activity has yet to be confirmed. OS occurs when cellular antioxidants are overwhelmed by a surplus generation of reactive oxygen species (ROS), which in PD, is possibly caused by a number of factors including the reactive metabolites of dopamine and alterations in the level of iron as well as neuro-inflammation and MRC dysfunction in the substantia nigra and mid-brain regions. In addition, perturbations in glutathione metabolism and the pentose phosphate pathway may also contribute to the OS associated with PD.

This Special Issue aims to highlight appropriate antioxidant therapeutic strategies that ameliorate OS in disease and target the mitochondria. This Special Issue will also focus on suitable low-invasive methods to assess evidence of OS in patients and their application to disease monitoring.

Dr. Iain P. Hargreaves
Guest Editor

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Keywords

  • Parkinson’s disease (PD)
  • reactive oxygen species (ROS)
  • oxidative stress (OS)
  • mitochondrial respiratory chain (MRC)
  • mitochondrial dysfunction
  • glutathione, pentose phosphate pathway

Published Papers (2 papers)

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Research

21 pages, 2048 KiB  
Article
The Effect of Neuronal CoQ10 Deficiency and Mitochondrial Dysfunction on a Rotenone-Induced Neuronal Cell Model of Parkinson’s Disease
by Lauren Millichap, Nadia Turton, Elisabetta Damiani, Fabio Marcheggiani, Patrick Orlando, Sonia Silvestri, Luca Tiano and Iain P. Hargreaves
Int. J. Mol. Sci. 2024, 25(12), 6622; https://doi.org/10.3390/ijms25126622 - 16 Jun 2024
Viewed by 255
Abstract
Parkinson’s disease (PD) is the second most prevalent neurodegenerative disorder currently affecting the ageing population. Although the aetiology of PD has yet to be fully elucidated, environmental factors such as exposure to the naturally occurring neurotoxin rotenone has been associated with an increased [...] Read more.
Parkinson’s disease (PD) is the second most prevalent neurodegenerative disorder currently affecting the ageing population. Although the aetiology of PD has yet to be fully elucidated, environmental factors such as exposure to the naturally occurring neurotoxin rotenone has been associated with an increased risk of developing PD. Rotenone inhibits mitochondrial respiratory chain (MRC) complex I activity as well as induces dopaminergic neuronal death. The aim of the present study was to investigate the underlying mechanisms of rotenone-induced mitochondrial dysfunction and oxidative stress in an in vitro SH-SY5Y neuronal cell model of PD and to assess the ability of pre-treatment with Coenzyme Q10 (CoQ10) to ameliorate oxidative stress in this model. Spectrophotometric determination of the mitochondrial enzyme activities and fluorescence probe studies of reactive oxygen species (ROS) production was assessed. Significant inhibition of MRC complex I and II-III activities was observed, together with a significant loss of neuronal viability, CoQ10 status, and ATP synthesis. Additionally, significant increases were observed in intracellular and mitochondrial ROS production. Remarkably, CoQ10 supplementation was found to reduce ROS formation. These results have indicated mitochondrial dysfunction and increased oxidative stress in a rotenone-induced neuronal cell model of PD that was ameliorated by CoQ10 supplementation. Full article
14 pages, 2201 KiB  
Article
Parkinson’s Disease Dementia Patients: Expression of Glia Maturation Factor in the Brain
by Ramasamy Thangavel, Harleen Kaur, Iuliia Dubova, Govindhasamy Pushphavathi Selvakumar, Mohammad Ejaz Ahmed, Sudhanshu P. Raikwar, Raghav Govindarajan and Duraisamy Kempuraj
Int. J. Mol. Sci. 2024, 25(2), 1182; https://doi.org/10.3390/ijms25021182 - 18 Jan 2024
Cited by 1 | Viewed by 1071
Abstract
Parkinson’s disease (PD) is the second most common progressive neurodegenerative disease characterized by the presence of dopaminergic neuronal loss and motor disorders. PD dementia (PDD) is a cognitive disorder that affects many PD patients. We have previously demonstrated the proinflammatory role of the [...] Read more.
Parkinson’s disease (PD) is the second most common progressive neurodegenerative disease characterized by the presence of dopaminergic neuronal loss and motor disorders. PD dementia (PDD) is a cognitive disorder that affects many PD patients. We have previously demonstrated the proinflammatory role of the glia maturation factor (GMF) in neuroinflammation and neurodegeneration in AD, PD, traumatic brain injury (TBI), and experimental autoimmune encephalomyelitis (EAE) in human brains and animal models. The purpose of this study was to investigate the expression of the GMF in the human PDD brain. We analyzed the expression pattern of the GMF protein in conjunction with amyloid plaques (APs) and neurofibrillary tangles (NFTs) in the substantia nigra (SN) and striatum of PDD brains using immunostaining. We detected a large number of GMF-positive glial fibrillary acidic protein (GFAP) reactive astrocytes, especially abundant in areas with degenerating dopaminergic neurons within the SN and striatum in PDD. Additionally, we observed excess levels of GMF in glial cells in the vicinity of APs, and NFTs in the SN and striatum of PDD and non-PDD patients. We found that the majority of GMF-positive immunoreactive glial cells were co-localized with GFAP-reactive astrocytes. Our findings suggest that the GMF may be involved in the pathogenesis of PDD. Full article
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