ReviewJournal of bioenergetics and biomembranes2011
Mitochondrial dysfunction in familial amyotrophic lateral sclerosis.
Review in Journal of bioenergetics and biomembranes, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
22 citing papers in PubMed, 31 citations in OpenAlex.
- Potential Applications for Growth Hormone Secretagogues Treatment of Amyotrophic Lateral Sclerosis.Current neuropharmacology · 2023Article
- The protective role of exercise against age-related neurodegeneration.Ageing research reviews · 2022Review
- Prevention of mitochondrial impairment by inhibition of protein phosphatase 1 activity in amyotrophic lateral sclerosis.Cell death & disease · 2020Article
- Dysregulated mitochondrial CaArchives of biochemistry and biophysics · 2019Review
- The Role of Exercise as a Non-pharmacological Therapeutic Approach for Amyotrophic Lateral Sclerosis: Beneficial or Detrimental?Frontiers in neurology · 2019Review
- Nrf2 Signaling in Sodium Azide-Treated Oligodendrocytes Restores Mitochondrial Functions.Journal of molecular neuroscience : MN · 2018Article
- Inhibition of Drp1/Fis1 interaction slows progression of amyotrophic lateral sclerosis.EMBO molecular medicine · 2018Article
- Prevention of Hippocampal Neuronal Damage and Cognitive Function Deficits in Vascular Dementia by Dextromethorphan.Molecular neurobiology · 2016Article
- Cerebrospinal Fluid from Sporadic Amyotrophic Lateral Sclerosis Patients Induces Mitochondrial and Lysosomal Dysfunction.Neurochemical research · 2016Article
- Mitochondrial Disorders May Mimic Amyotrophic Lateral Sclerosis at Onset.Sultan Qaboos University medical journal · 2016Article
- Deficiency of the zinc finger protein ZFP106 causes motor and sensory neurodegeneration.Human molecular genetics · 2016Article
- Skeletal Muscle Satellite Cells, Mitochondria, and MicroRNAs: Their Involvement in the Pathogenesis of ALS.Frontiers in physiology · 2016Review
- A novel SOD1-ALS mutation separates central and peripheral effects of mutant SOD1 toxicity.Human molecular genetics · 2015Article
- Resveratrol: A Focus on Several Neurodegenerative Diseases.Oxidative medicine and cellular longevity · 2015Review
- Bioenergetic markers in skin fibroblasts of sporadic amyotrophic lateral sclerosis and progressive lateral sclerosis patients.Annals of neurology · 2014Article
- Huntingtin protein is essential for mitochondrial metabolism, bioenergetics and structure in murine embryonic stem cells.Developmental biology · 2014Article
- Adaptive cellular stress pathways as therapeutic targets of dietary phytochemicals: focus on the nervous system.Pharmacological reviews · 2014Review
- Abnormal mitochondrial transport and morphology are common pathological denominators in SOD1 and TDP43 ALS mouse models.Human molecular genetics · 2014Article
- Is SOD1 loss of function involved in amyotrophic lateral sclerosis?Brain : a journal of neurology · 2013Review
- Iron and copper in mitochondrial diseases.Cell metabolism · 2013Article
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A growing body of evidence suggests that mitochondrial dysfunctions play a crucial role in the pathogenesis of various neurodegenerative disorders, including amyotrophic lateral sclerosis (ALS), a neurodegenerative disease affecting both upper and lower motor neurons. Although ALS is predominantly a sporadic disease, approximately 10% of cases are familial. The most frequent familial form is caused by mutations in the gene encoding Cu/Zn superoxide dismutase 1 (SOD1). A dominant toxic gain of function of mutant SOD1 has been considered as the cause of the disease and mitochondria are thought to be key players in the pathogenesis. However, the exact nature of the link between mutant SOD1 and mitochondrial dysfunctions remains to be established. Here, we briefly review the evidence for mitochondrial dysfunctions in familial ALS and discuss a possible link between mutant SOD1 and mitochondrial dysfunction.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.