ReviewFrontiers in cellular neuroscience2015
Oxidative stress and mitochondrial damage: importance in non-SOD1 ALS.
Review in Frontiers in cellular neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
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Who cites it
64 citing papers in PubMed, 139 citations in OpenAlex.
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- Amyotrophic Lateral Sclerosis: Pathophysiological Mechanisms and Treatment Strategies (Part 2).International journal of molecular sciences · 2025Review
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- Emerging Ferroptosis Involvement in Amyotrophic Lateral Sclerosis Pathogenesis: Neuroprotective Activity of Polyphenols.Molecules (Basel, Switzerland) · 2025Review
- Association between cardiometabolic diseases and the risk and progression of motor neuron diseases in Sweden: a population-based case-control study.The Lancet regional health. Europe · 2025Article
- VDAC1: A Key Player in the Mitochondrial Landscape of Neurodegeneration.Biomolecules · 2024Review
- Embryotrophic effect of exogenous protein contained adipose-derived stem cell extracellular vesicles.Journal of animal science and biotechnology · 2024Article
- Identification of Novel Biomarkers Using Serum and Urinary Proteomics for Early Detection of Hypoxic Ischemic Encephalopathy.Indian journal of clinical biochemistry : IJCB · 2024Article
- Advancements in Pharmacological Interventions and Novel Therapeutic Approaches for Amyotrophic Lateral Sclerosis.Biomedicines · 2024Review
- Revisiting Glutamate Excitotoxicity in Amyotrophic Lateral Sclerosis and Age-Related Neurodegeneration.International journal of molecular sciences · 2024Review
- Mitochondria Dysfunction and Neuroinflammation in Neurodegeneration: Who Comes First?Antioxidants (Basel, Switzerland) · 2024Review
- Effects of 8 days intake of hydrogen-rich water on muscular endurance performance and fatigue recovery during resistance training.Frontiers in physiology · 2024Article
- Physical exercise in amyotrophic lateral sclerosis: a potential co-adjuvant therapeutic option to counteract disease progression.Frontiers in cell and developmental biology · 2024Review
- Short-term outcome of plasma adsorption therapy in amyotrophic lateral sclerosis.Journal of medical biochemistry · 2023Article
- Altered Metabolism in Motor Neuron Diseases: Mechanism and Potential Therapeutic Target.Cells · 2023Review
- Review
- Modulation of histone H3K4 dimethylation by spermidine ameliorates motor neuron survival and neuropathology in a mouse model of ALS.Journal of biomedical science · 2022Article
- Review
- Oxidative Stress in Amyotrophic Lateral Sclerosis: Synergy of Genetic and Environmental Factors.International journal of molecular sciences · 2022Review
- The use of fibroblasts as a valuable strategy for studying mitochondrial impairment in neurological disorders.Translational neurodegeneration · 2022Review
4 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It is well known that mitochondrial damage (MD) is both the major contributor to oxidative stress (OS) (the condition arising from unbalance between production and removal of reactive oxygen species) and one of the major consequences of OS, because of the high dependance of mitochondrial function on redox-sensitive targets such as intact membranes. Conditions in which neuronal cells are not able to cope with MD and OS seem to lead or contribute to several neurodegenerative diseases including Amyotrophic Lateral Sclerosis (ALS), at least in the most studied superoxide dismutase 1 (SOD1)-linked genetic variant. As summarized in this review, new evidence indicates that MD and OS play a role also in non-SOD1 ALS and thus they may represent a target for therapy despite previous failures in clinical trials.
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