Oxidative Stress and Mitochondrial Dysfunction in Huntington’s and Other Neurodegenerative Diseases

2017 ◽  
pp. 159-170
Keyword(s):  
Oxidative Stress ◽  
Neurodegenerative Diseases ◽  
Mitochondrial Dysfunction

Oxidative stress, mitochondrial dysfunction and neurodegenerative diseases; a mechanistic insight

2015 ◽  
Vol 74 ◽  
pp. 101-110 ◽  
Author(s):  
Aashiq Hussain Bhat ◽  
Khalid Bashir Dar ◽  
Suhail Anees ◽  
Mohammad Afzal Zargar ◽  
Akbar Masood ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Neurodegenerative Diseases ◽  
Mitochondrial Dysfunction ◽  
Mechanistic Insight

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 Insights into the Pathogenesis of Neurodegenerative Diseases: Focus on Mitochondrial Dysfunction and Oxidative Stress

2021 ◽  
Vol 22 (21) ◽  
pp. 11847
Author(s):  
Anamaria Jurcau
Keyword(s):  
Oxidative Stress ◽  
Clinical Trials ◽  
Neurodegenerative Diseases ◽  
Mitochondrial Dysfunction ◽  
Healthy Lifestyle ◽  
Aggressive Therapy ◽  
Slowing Down ◽  
Familial Cases ◽  
And Oxidative Stress ◽  
Lateral Sclerosis

As the population ages, the incidence of neurodegenerative diseases is increasing. Due to intensive research, important steps in the elucidation of pathogenetic cascades have been made and significantly implicated mitochondrial dysfunction and oxidative stress. However, the available treatment in Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis is mainly symptomatic, providing minor benefits and, at most, slowing down the progression of the disease. Although in preclinical setting, drugs targeting mitochondrial dysfunction and oxidative stress yielded encouraging results, clinical trials failed or had inconclusive results. It is likely that by the time of clinical diagnosis, the pathogenetic cascades are full-blown and significant numbers of neurons have already degenerated, making it impossible for mitochondria-targeted or antioxidant molecules to stop or reverse the process. Until further research will provide more efficient molecules, a healthy lifestyle, with plenty of dietary antioxidants and avoidance of exogenous oxidants may postpone the onset of neurodegeneration, while familial cases may benefit from genetic testing and aggressive therapy started in the preclinical stage.

scholarly journals Air Pollution-Related Brain Metal Dyshomeostasis as a Potential Risk Factor for Neurodevelopmental Disorders and Neurodegenerative Diseases

Atmosphere ◽  
2020 ◽  
Vol 11 (10) ◽  
pp. 1098
Author(s):  
Deborah Cory-Slechta ◽  
Marissa Sobolewski ◽  
Günter Oberdörster
Keyword(s):  
Oxidative Stress ◽  
Air Pollution ◽  
Cell Death ◽  
Neurodegenerative Diseases ◽  
Mitochondrial Dysfunction ◽  
Neurodevelopmental Disorders ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Autism Spectrum ◽  
System Structure

Increasing evidence links air pollution (AP) exposure to effects on the central nervous system structure and function. Particulate matter AP, especially the ultrafine (nanoparticle) components, can carry numerous metal and trace element contaminants that can reach the brain in utero and after birth. Excess brain exposure to either essential or non-essential elements can result in brain dyshomeostasis, which has been implicated in both neurodevelopmental disorders (NDDs; autism spectrum disorder, schizophrenia, and attention deficit hyperactivity disorder) and neurodegenerative diseases (NDGDs; Alzheimer’s disease, Parkinson’s disease, multiple sclerosis, and amyotrophic lateral sclerosis). This review summarizes the current understanding of the extent to which the inhalational or intranasal instillation of metals reproduces in vivo the shared features of NDDs and NDGDs, including enlarged lateral ventricles, alterations in myelination, glutamatergic dysfunction, neuronal cell death, inflammation, microglial activation, oxidative stress, mitochondrial dysfunction, altered social behaviors, cognitive dysfunction, and impulsivity. Although evidence is limited to date, neuronal cell death, oxidative stress, and mitochondrial dysfunction are reproduced by numerous metals. Understanding the specific contribution of metals/trace elements to this neurotoxicity can guide the development of more realistic animal exposure models of human AP exposure and consequently lead to a more meaningful approach to mechanistic studies, potential intervention strategies, and regulatory requirements.

scholarly journals Linalool attenuates cell death against oxidative stress and mitochondrial dysfunction in neurodegenerative diseases

IBRO Reports ◽  
2019 ◽  
Vol 6 ◽  
pp. S366
Author(s):  
Angelica Maria Sabogal Guaqueta ◽  
Fabian Hobbie ◽  
Asmaa Oun ◽  
Erik Boddeke ◽  
Gloria Patricia Cardona Gomez ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Neurodegenerative Diseases ◽  
Mitochondrial Dysfunction

scholarly journals Oxidative Toxicity in Neurodegenerative Diseases: Role of Mitochondrial Dysfunction and Therapeutic Strategies

2011 ◽  
Vol 2011 ◽  
pp. 1-12 ◽  
Author(s):  
Katie Facecchia ◽  
Lee-Anne Fochesato ◽  
Sidhartha D. Ray ◽  
Sidney J. Stohs ◽  
Siyaram Pandey
Keyword(s):  
Oxidative Stress ◽  
Neurodegenerative Diseases ◽  
Mitochondrial Dysfunction ◽  
Mammalian Cells ◽  
Defense Mechanisms ◽  
Neuronal Loss ◽  
Work Related ◽  
Antioxidative Agents ◽  
The Central Nervous System ◽  
Mitochondrial Membrane Permeabilization

Besides fluorine, oxygen is the most electronegative element with the highest reduction potential in biological systems. Metabolic pathways in mammalian cells utilize oxygen as the ultimate oxidizing agent to harvest free energy. They are very efficient, but not without risk of generating various oxygen radicals. These cells have good antioxidative defense mechanisms to neutralize these radicals and prevent oxidative stress. However, increased oxidative stress results in oxidative modifications in lipid, protein, and nucleic acids, leading to mitochondrial dysfunction and cell death. Oxidative stress and mitochondrial dysfunction have been implicated in many neurodegenerative disorders including Alzheimer's disease, Parkinson's disease, and stroke-related brain damage. Research has indicated mitochondria play a central role in cell suicide. An increase in oxidative stress causes mitochondrial dysfunction, leading to more production of reactive oxygen species and eventually mitochondrial membrane permeabilization. Once the mitochondria are destabilized, cells are destined to commit suicide. Therefore, antioxidative agents alone are not sufficient to protect neuronal loss in many neurodegenerative diseases. Combinatorial treatment with antioxidative agents could stabilize mitochondria and may be the most suitable strategy to prevent neuronal loss. This review discusses recent work related to oxidative toxicity in the central nervous system and strategies to treat neurodegenerative diseases.

Are oxidative stress and mitochondrial dysfunction the key players in the neurodegenerative diseases?

2012 ◽  
Vol 46 (11) ◽  
pp. 1327-1338 ◽  
Author(s):  
Marta Di Carlo ◽  
Daniela Giacomazza ◽  
Pasquale Picone ◽  
Domenico Nuzzo ◽  
Pier Luigi San Biagio
Keyword(s):  
Oxidative Stress ◽  
Neurodegenerative Diseases ◽  
Mitochondrial Dysfunction ◽  
Key Players
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