Oxidative stress, mitochondrial damage and neurodegenerative diseases

By Chunyan Guo, Li Sun, Xueping Chen, Dan-shen Zhang. Neural Regeneration Research, 2013

1,234 citations recorded by the source corpus.

Oxidative stress and mitochondrial damage have been implicated in the pathogenesis of several neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease and amyotrophic lateral sclerosis. Oxidative stress is characterized by the overproduction of reactive oxygen species, which can induce mitochondrial DNA mutations, damage the mitochondrial respiratory chain, alter membrane permeability, and influence Ca2+ homeostasis and mitochondrial defense systems. All these changes are implicated in the development of these neurodegenerative diseases, mediating or amplifying neuronal dysfunction and triggering neurodegeneration. This paper summarizes the contribution of oxidative stress and mitochondrial damage to the onset of neurodegenerative eases and discusses strategies to modify mitochondrial dysfunction that may be attractive therapeutic interventions for the treatment of various neurodegenerative diseases.

Subfields: Biochemistry, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/5a4d7028f82a12defd81a45565b975a85e4d5f93

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In Biochemistry

1. Shrikant Kukreti
2. Anju Singh
3. R. Kukreti
4. L. Saso

In Molecular Biology

1. Shrikant Kukreti
2. Anju Singh
3. R. Kukreti
4. L. Saso

In Physiology

1. M. T. Islam

Citations in the corpus

• Oxidative Stress: A Key Modulator in Neurodegenerative Diseases (2019, background): “ROS can cause mitochondrial DNA mutations, membrane permeability, and calcium homeostasis, as well as enhance the oxidation of lipids and protein carbonylation, thus leading to various neurodegenerative diseases including ALS [126,127].”
• Oxidative stress and mitochondrial dysfunction-linked neurodegenerative disorders (2017, background): “[25] A common pathway of reactive species-mediated mitochondrial events is shown in Figure 3.”
• The Advancing of Zinc Oxide Nanoparticles for Biomedical Applications (2018, background): “However, excessive ROS will lead to mitochondrial damage and result in the loss of protein activity balance that finally causes cell apoptosis [60].”