scholarly journals Parkinson's Disease in Relation to Pesticide Exposure and Nuclear Encoded Mitochondrial Complex I Gene Variants

2006 ◽  
Vol 2006 ◽  
pp. 1-8 ◽  
Author(s):  
Elizabeth H. Corder ◽  
George D. Mellick
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Complex I ◽  
Pesticide Exposure ◽  
Neurodegenerative Disorder ◽  
Control Sample ◽  
Mitochondrial Complex I ◽  
Mitochondrial Complex ◽  
Age Related ◽  
I Gene

Parkinson's disease (PD) is a common age-related neurodegenerative disorder thought to result from the integrated effects of genetic background and exposure to neuronal toxins. Certain individual nuclear-encoded mitochondrial complex I gene polymorphisms were found to be associated with∼2-fold risk variation in an Australian case-control sample. We further characterized this sample of306cases and321controls to determine the mutual information contained in the22SNPs and, additionally, level of pesticide exposure: five distinct risk sets were identified using grade-of-membership analysis. Of these, one was robust to pesticide exposure (I), three were vulnerable (II, III, IV), and another (V) denoted low risk for unexposed persons. Risk for individual subjects varied>16-fold according to level of membership in the vulnerable groups. We conclude that inherited variation in mitochondrial complex I genes and pesticide exposure together modulate risk for PD.

scholarly journals A novel neuroprotective therapy for Parkinson’s disease using a viral noncoding RNA that protects mitochondrial Complex I activity

2011 ◽  
Vol 209 (1) ◽  
pp. 1-10 ◽  
Author(s):  
Wei-Li Kuan ◽  
Emma Poole ◽  
Michael Fletcher ◽  
Sharon Karniely ◽  
Pam Tyers ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Complex I ◽  
Neurodegenerative Disorder ◽  
Dopamine Neurons ◽  
Mitochondrial Complex I ◽  
Mitochondrial Complex ◽  
Neuroprotective Therapy ◽  
Nigrostriatal Dopamine Neurons ◽  
Complex I Activity

Parkinson’s disease (PD) is a neurodegenerative disorder that results in the loss of nigrostriatal dopamine neurons. The etiology of this cell loss is unknown, but it involves abnormalities in mitochondrial function. In this study, we have demonstrated that the administration of a novel noncoding p137 RNA, derived from the human cytomegaloviral β2.7 transcript, can prevent and rescue dopaminergic cell death in vitro and in animal models of PD by protecting mitochondrial Complex I activity. Furthermore, as this p137 RNA is fused to a rabies virus glycoprotein peptide that facilitates delivery of RNA across the blood–brain barrier, such protection can be achieved through a peripheral intravenous administration of this agent after the initiation of a dopaminergic lesion. This approach has major implications for the potential treatment of PD, especially given that this novel agent could have the same protective effect on all diseased neurons affected as part of this disease process, not just the dopaminergic nigrostriatal pathway.

scholarly journals Mitochondrial Complex I Reversible S-Nitrosation Improves Bioenergetics and Is Protective in Parkinson's Disease

2018 ◽  
Vol 28 (1) ◽  
pp. 44-61 ◽  
Author(s):  
Chiara Milanese ◽  
Victor Tapias ◽  
Sylvia Gabriels ◽  
Silvia Cerri ◽  
Giovanna Levandis ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Complex I ◽  
Mitochondrial Complex I ◽  
Mitochondrial Complex

scholarly journals Bacopa monnieri Phytochemicals Mediated Synthesis of Platinum Nanoparticles and Its Neurorescue Effect on 1-Methyl 4-Phenyl 1,2,3,6 Tetrahydropyridine-Induced Experimental Parkinsonism in Zebrafish

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Jayshree Nellore ◽  
Cynthia Pauline ◽  
Kanchana Amarnath
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Platinum Nanoparticles ◽  
Complex I ◽  
Leaf Extract ◽  
Bacopa Monnieri ◽  
Mitochondrial Complex I ◽  
Mitochondrial Complex ◽  
Zebrafish Model ◽  
Experimental Parkinsonism

Current discovery demonstrates the rapid formation of platinum nanoparticles using leaf extract of a neurobeneficial plant, Bacopa monnieri (BmE). The nanoparticles (BmE-PtNPs) were stabilized and then coated with varied phytochemicals present within the leaf extract. These nanoparticles demonstrated the same activity of Complex I, as that of oxidizing NADH to NAD+ using a spectrophotometric method. This suggests that BmE-PtNPs are a potential medicinal substance for oxidative stress mediated disease with suppressed mitochondrial complex I, namely, Parkinson's disease (PD). Hence, the neuroprotective potentials of the phytochemical coated nanoparticle were explored in 1-methyl 4-phenyl 1,2,3,6 tetrahydropyridine- (MPTP-)induced experimental Parkinsonism in zebrafish model. BmE-PtNPs pretreatment significantly reversed toxic effects of MPTP by increasing the levels of dopamine, its metabolites, GSH and activities of GPx, catalase, SOD and complex I, and reducing levels of MDA along with enhanced locomotor activity. Taken together, these findings suggest that BmE-PtNPs have protective effect in MPTP-induced neurotoxicity in this model of Parkinson's disease via their dual functions as mitochondrial complex I and antioxidant activity.

scholarly journals Parkinson’s disease and mitochondrial complex I: a perspective on the Ndi1 therapy

2009 ◽  
Vol 41 (6) ◽  
pp. 493-497 ◽  
Author(s):  
Mathieu Marella ◽  
Byoung Boo Seo ◽  
Takao Yagi ◽  
Akemi Matsuno-Yagi
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Complex I ◽  
Mitochondrial Complex I ◽  
Mitochondrial Complex

scholarly journals Maternally Inherited Differences within Mitochondrial Complex I Control Murine Healthspan

Genes ◽  
2019 ◽  
Vol 10 (7) ◽  
pp. 532
Author(s):  
Misa Hirose ◽  
Paul Schilf ◽  
Kim Zarse ◽  
Hauke Busch ◽  
Georg Fuellen ◽  
...  
Keyword(s):  
Experimental Evidence ◽  
Complex I ◽  
Association Studies ◽  
Mitochondrial Complex I ◽  
Enzyme Complex ◽  
Mitochondrial Complex ◽  
Age Related ◽  
Functional Relevance ◽  
Invertebrate Models ◽  
I Gene

Mitochondrial complex I—the largest enzyme complex of the mitochondrial oxidative phosphorylation machinery—has been proposed to contribute to a variety of age-related pathological alterations as well as longevity. The enzyme complex-consisting proteins are encoded by both nuclear (nDNA) and mitochondrial DNA (mtDNA). While some association studies of mtDNA encoded complex I genes and lifespan in humans have been reported, experimental evidence and the functional consequence of such variants is limited to studies using invertebrate models. Here, we present experimental evidence that a homoplasmic mutation in the mitochondrially encoded complex I gene mt-Nd2 modulates lifespan by altering cellular tryptophan levels and, consequently, ageing-related pathways in mice. A conplastic mouse strain carrying a mutation at m.4738C > A in mt-Nd2 lived slightly, but significantly, shorter than the controls did. The same mutation led to a higher susceptibility to glucose intolerance induced by high-fat diet feeding. These phenotypes were not observed in mice carrying a mutation in another mtDNA encoded complex I gene, mt-Nd5, suggesting the functional relevance of particular mutations in complex I to ageing and age-related diseases.

Mitochondrial Complex I Deficiency in Parkinson's Disease

1990 ◽  
Vol 54 (3) ◽  
pp. 823-827 ◽  
Author(s):  
A. H. V. Schapira ◽  
J. M. Cooper ◽  
D. Dexter ◽  
J. B. Clark ◽  
P. Jenner ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Complex I ◽  
Mitochondrial Complex I ◽  
Mitochondrial Complex ◽  
Complex I Deficiency
Sign in / Sign up

Export Citation Format

Share Document