ReviewInternational journal of molecular sciences2018
SOD1 in Amyotrophic Lateral Sclerosis: "Ambivalent" Behavior Connected to the Disease.
Review in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers, 2 of them syntheses that pooled it.
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.
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Who cites it
77 citing papers in PubMed, 2 syntheses or guidelines pooled it, 154 citations in OpenAlex.
- Exploring Genetic Therapies Targeting Amyotrophic Lateral Sclerosis in Animal Models: A Systematic Review and Meta-Analysis.The journal of gene medicine · 2026Pooled it
- Superoxide Dismutase Administration: A Review of Proposed Human Uses.Molecules (Basel, Switzerland) · 2021Pooled it
- Review
- Amyotrophic Lateral Sclerosis (ALS) Genetics and Microbiota: A Comprehensive Review.International journal of molecular sciences · 2026Review
- Impaired nucleocytoplasmic transport in SOD1-mediated ALS.Molecular neurodegeneration · 2026Article
- The HDAC Inhibitor Butyrate Reduces SOD1 Aggregation and Improves Motor Function inInternational journal of cell biology · 2026Article
- Integrative analysis of transcriptomics and drug-target networks identifies SMN1 as a novel biomarker and therapeutic target for amyotrophic lateral sclerosis.Journal, genetic engineering & biotechnology · 2025Article
- Impact of SOD1 Transcript Variants on Amyotrophic Lateral Sclerosis Severity.International journal of molecular sciences · 2025Article
- Research progress of extracellular vesicles derived from mesenchymal stem cells in the treatment of neurodegenerative diseases.Frontiers in immunology · 2025Review
- Copper homeostasis and cuproptosis: implications for neurodegenerative diseases.Frontiers in aging neuroscience · 2025Review
- GeneCOCOA: Detecting context-specific functions of individual genes using co-expression data.PLoS computational biology · 2025Article
- Studying the mechanisms of neurodegeneration:Frontiers in cellular neuroscience · 2025Review
- Nuclear Localization of Human SOD1 in Motor Neurons in Mouse Model and Patient Amyotrophic Lateral Sclerosis: Possible Links to Cholinergic Phenotype, NADPH Oxidase, Oxidative Stress, and DNA Damage.International journal of molecular sciences · 2024Article
- Aberrant protein aggregation in amyotrophic lateral sclerosis.Journal of neurology · 2024Review
- Increased copy-number variant load of associated risk genes in sporadic cases of amyotrophic lateral sclerosis.Cellular and molecular life sciences : CMLS · 2024Article
- Chemical composition and toxicity studies onRSC advances · 2024Article
- Amyotrophic Lateral Sclerosis-Associated Mutants of SOD1 Perturb mRNA Splicing through Aberrant Interactions with SRSF2.Analytical chemistry · 2024Article
- DYNATE: Localizing rare-variant association regions via multiple testing embedded in an aggregation tree.Genetic epidemiology · 2024Article
- Acetyl-L-carnitine and Amyotrophic Lateral Sclerosis: Current Evidence and Potential use.CNS & neurological disorders drug targets · 2024Review
- Advancements and challenges in amyotrophic lateral sclerosis.Frontiers in neuroscience · 2024Review
17 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In 1993, Rosen and collaborators discovered that the gene encoding SOD1 has mutations in amyotrophic lateral sclerosis (ALS) patients; moreover, these mutations are found in the exon regions, suggesting that their toxic effects are the consequence of protein dysfunction with an increase of oxidative stress. While a clear genetic picture has been delineated, a more complex scenario has been ascribed to the SOD1 protein. On the one hand, some evidence sustains the hypothesis of an additionally toxic role for wild-type SOD1 (WT-SOD1) in the pathogenesis of sporadic ALS. On the other hand, our group identified a discrepancy among WT-SOD1 protein expression levels and mRNA in ALS sporadic patients, thus providing the hypothesis of a re-localization of the “missing” SOD1 in a different sub-cellular compartment, i.e., nucleus, or an aggregation/precipitation in the insoluble fraction. Moreover, our data also indicate an association between longer disease duration and higher amounts of soluble SOD1 within the nucleus, suggesting a possible defensive role of the protein in this compartment. Starting from this evidence, in this review we will attempt to resolve the “ambivalent” behavior of SOD1 in ALS disease and we will try to classify sporadic ALS patients according to a novel biological signature, i.e., SOD localization.
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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.