A Review on Mitochondrial Dysfunction and Oxidative stress due to Complex-Ⅰ in Parkinson Disease

2021 ◽  
pp. 167-170
Author(s):  
V Nuthan Kumar Babu ◽  
Navneet Khurana
Keyword(s):  
Oxidative Stress ◽  
Parkinson Disease ◽  
Mitochondrial Dysfunction ◽  
Neurodegenerative Disorder ◽  
Dimethyl Fumarate ◽  
World Population ◽  
Emerging Therapies ◽  
And Oxidative Stress ◽  
Transplantation Therapy

Parkinson’s disease (PD) is the common physical movement disorder, and it is 2nd most progressive widespread neurodegenerative disorder all over the world, and it is reported that and essential 10 million, over 0.3 % of the total world population. A thoughtful reduction of the neurotransmitter dopamine (DA) in the striatum is the main cause of these motor symptoms, collectively known as parkinsonism. Mitochondria serves as most important organelle in most of the cells and are essential for life and it is also called as heart for all cellular metabolisms. The main and most important role of mitochondria is generation of ATP via oxidative phosphorylation. In this study will study about how complex Ⅰ deficiency effects the mitochondrial and oxidative stress and reactive oxygen species which cause mitochondrial dysfunction and we also study emerging therapies for Parkinson disease with the help of coenzyme Q10 and some genes like FUN-14, FUNDC-1 and dimethyl fumarate or BG-12 in some phases of clinical trials and also by cell transplantation therapy and in future this study helps in finding how this sporadic Parkinson disease occurs in parkinsonism.

scholarly journals Alzheimer’s Pathogenesis and Its Link to the Mitochondrion

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
C. Simoncini ◽  
D. Orsucci ◽  
E. Caldarazzo Ienco ◽  
G. Siciliano ◽  
U. Bonuccelli ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dysfunction ◽  
Cognitive Functions ◽  
Neurodegenerative Disorder ◽  
The Elderly ◽  
Mitochondria Dysfunction ◽  
Neurodegenerative Process ◽  
Mitochondrial Impairment ◽  
And Oxidative Stress

Alzheimer’s disease (AD) is the most common form of dementia in the elderly. This neurodegenerative disorder is clinically characterized by impairment of cognitive functions and changes in behaviour and personality. The pathogenesis of AD is still unclear. Recent evidence supports some role of mitochondria dysfunction and oxidative stress in the development of the neurodegenerative process. In this review, we discuss the role of mitochondrial dysfunction in AD, focusing on the mechanisms that lead to mitochondrial impairment, oxidative stress, and neurodegeneration, a “vicious circle” that ends in dementia.

scholarly journals The role of mitochondria-targeted antioxidant MitoQ in neurodegenerative disease

2018 ◽  
pp. 1-8
Author(s):  
Linlin Zhang ◽  
Aurelio Reyes ◽  
Xiangdong Wang
Keyword(s):  
Oxidative Stress ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Neurodegenerative Diseases ◽  
Mitochondrial Dysfunction ◽  
Neurodegenerative Disease ◽  
Amyloid Β ◽  
Amyloid Β Peptide ◽  
And Oxidative Stress

Abstract: The discovery of charged molecules being able to cross the mitochondrial membrane has prompted many scholars to exploit this idea to find a way of preventing or slowing down aging. In this paper, we will focus on mitochondriatargeted antioxidants, which are cationic derivatives of plastoquinone, and in particular on the mitochondria-targeted antioxidant therapy of neurodegenerative diseases. It is well known that the accumulation of amyloid-β peptide (Aβ) in mitochondria and its related mitochondrial dysfunction are critical signatures of Alzheimer’ s disease (AD). In another neurodegenerative disease, Parkinson’s disease (PD), the loss of dopaminergic neurons in the substantia nigra and the production of Lewy bodies are among their pathological features. Pathogenesis of Parkinson’s disease and Alzheimer’s disease has been frequently linked to mitochondrial dysfunction and oxidative stress. Recent studies show that MitoQ, a mitochondria-targeted antioxidant, may possess therapeutic potential for Aβ-related and oxidative stress-associated neurodegenerative diseases, especially AD. Although MitoQ has been developed to the stage of clinical trials in PD, its true clinical effect still need further verification. This review aims to discuss the role of mitochondrial pathology in neurodegenerative diseases, as well as the recent development of mitochondrial targeted antioxidants as a potential treatment for these diseases by removing excess oxygen free radicals and inhibiting lipid peroxidation in order to improve mitochondrial function.  

scholarly journals The potential role of neuroinflammation and transcription factors in Parkinson disease

2017 ◽  
Vol 19 (1) ◽  
pp. 71-80 ◽  
Keyword(s):  
Oxidative Stress ◽  
Transcription Factors ◽  
Substantia Nigra ◽  
Parkinson Disease ◽  
Signaling Pathways ◽  
Dopaminergic Neurons ◽  
Neurodegenerative Disorder ◽  
Brain Regions ◽  
Death Domain

Parkinson disease (PD) is a neurodegenerative disorder characterized by dopaminergic neurons affected by inflammatory processes. Post-mortem analyses of brain and cerebrospinal fluid from PD patients show the accumulation of proinflammatory cytokines, confirming an ongoing neuroinflammation in the affected brain regions. These inflammatory mediators may activate transcription factors—notably nuclear factor κB, Ying-Yang 1 (YY1), fibroblast growth factor 20 (FGF20), and mammalian target of rapamycin (mTOR)—which then regulate downstream signaling pathways that in turn promote death of dopaminergic neurons through death domain-containing receptors. Dopaminergic neurons are vulnerable to oxidative stress and inflammatory attack. An increased level of inducible nitric oxide synthase observed in the substantia nigra and striatum of PD patients suggests that both cytokine—and chemokine-induced toxicity and inflammation lead to oxidative stress that contributes to degeneration of dopaminergic neurons and to disease progression. Lipopolysaccharide activation of microglia in the proximity of dopaminergic neurons in the substantia nigra causes their degeneration, and this appears to be a selective vulnerability of dopaminergic neurons to inflammation. In this review, we will look at the role of various transcription factors and signaling pathways in the development of PD.

scholarly journals Oxidative Stress and Epilepsy: Literature Review

2012 ◽  
Vol 2012 ◽  
pp. 1-12 ◽  
Author(s):  
Carlos Clayton Torres Aguiar ◽  
Anália Barbosa Almeida ◽  
Paulo Victor Pontes Araújo ◽  
Rita Neuma Dantas Cavalcante de Abreu ◽  
Edna Maria Camelo Chaves ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Free Radicals ◽  
Mitochondrial Dysfunction ◽  
Experimental Studies ◽  
Cellular Damage ◽  
Brain Disorder ◽  
Chronic Oxidative Stress ◽  
Seizure Models ◽  
And Oxidative Stress

Backgrounds. The production of free radicals has a role in the regulation of biological function, cellular damage, and the pathogenesis of central nervous system conditions. Epilepsy is a highly prevalent serious brain disorder, and oxidative stress is regarded as a possible mechanism involved in epileptogenesis. Experimental studies suggest that oxidative stress is a contributing factor to the onset and evolution of epilepsy.Objective. A review was conducted to investigate the link between oxidative stress and seizures, and oxidative stress and age as risk factors for epilepsy. The role of oxidative stress in seizure induction and propagation is also discussed.Results/Conclusions. Oxidative stress and mitochondrial dysfunction are involved in neuronal death and seizures. There is evidence that suggests that antioxidant therapy may reduce lesions induced by oxidative free radicals in some animal seizure models. Studies have demonstrated that mitochondrial dysfunction is associated with chronic oxidative stress and may have an essential role in the epileptogenesis process; however, few studies have shown an established link between oxidative stress, seizures, and age.

Protective role of amantadine in mitochondrial dysfunction and oxidative stress mediated by hepatitis C virus protein expression

2014 ◽  
Vol 89 (4) ◽  
pp. 545-556 ◽  
Author(s):  
Giovanni Quarato ◽  
Rosella Scrima ◽  
Maria Ripoli ◽  
Francesca Agriesti ◽  
Darius Moradpour ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Protein Expression ◽  
Mitochondrial Dysfunction ◽  
Protective Role ◽  
Virus Protein ◽  
And Oxidative Stress

scholarly journals Human INCL fibroblasts display abnormal mitochondrial and lysosomal networks and heightened susceptibility to ROS-induced cell death

2020 ◽  
Author(s):  
Bailey Balouch ◽  
Halle Nagorsky ◽  
Truc Pham ◽  
Thai LaGraff ◽  
Quynh Chu-LaGraff
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Molecular Mechanisms ◽  
Neurodegenerative Disorder ◽  
Endoplasmic Reticulum Stress Response ◽  
Compound Heterozygous ◽  
Storage Material ◽  
Cellular Environment ◽  
And Oxidative Stress

AbstractInfantile Neuronal Ceroid Lipofuscinosis (INCL) is a pediatric neurodegenerative disorder characterized by progressive retinal and central nervous system deterioration during infancy. This lysosomal storage disorder results from a deficiency in the Palmitoyl Protein Thioesterase 1 (PPT1) enzyme - a lysosomal hydrolase which cleaves fatty acid chains such as palmitate from lipid-modified proteins. In the absence of PPT1 activity, these proteins fail to be degraded, leading to the accumulation of autofluorescence storage material in the lysosome. The underlying molecular mechanisms leading to INCL pathology remain poorly understood. A role for oxidative stress has been postulated, yet little evidence has been reported to support this possibility. Here we present a comprehensive cellular characterization of human PPT1-deficient fibroblast cells harboring Met1Ile and Tyr247His compound heterozygous mutations. We detected autofluorescence storage material and observed distinct organellar abnormalities of the lysosomal and mitochondrial structures, which supported previous postulations about the role of ER, mitochondria and oxidative stress in INCL. An increase in the number of lysosomal structures was found in INCL patient fibroblasts, which suggested an upregulation of lysosomal biogenesis, and an association with endoplasmic reticulum stress response. The mitochondrial network also displayed abnormal spherical punctate morphology instead of normal elongated tubules with extensive branching, supporting the involvement of mitochondrial and oxidative stress in INCL cell death. Autofluorescence accumulation and lysosomal pathologies can be mitigated in the presence of conditioned wild type media suggesting that a partial restoration via passive introduction of the enzyme into the cellular environment may be possible. We also demonstrated, for the first time, that human INCL fibroblasts have a heightened susceptibility to exogenous reactive oxygen species (ROS)-induced cell death, which suggested an elevated basal level of endogenous ROS in the mutant cell. Collectively, these findings support the role of intracellular organellar networks in INCL pathology, possibly due to oxidative stress.

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