ArticleFrontiers in molecular neuroscience2015
Mice Overexpressing Both Non-Mutated Human SOD1 and Mutated SOD1(G93A) Genes: A Competent Experimental Model for Studying Iron Metabolism in Amyotrophic Lateral Sclerosis.
Article in Frontiers in molecular neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 17 citations in OpenAlex.
- Pathological Sequelae Associated with Skeletal Muscle Atrophy and Histopathology in G93A*SOD1 Mice.Muscles (Basel, Switzerland) · 2023Article
- Chlorovirus ATCV-1 Accelerates Motor Deterioration in SOD1-G93A Transgenic Mice and Its SOD1 Augments Induction of Inflammatory Factors From Murine Macrophages.Frontiers in neurology · 2022Article
- Sex-dependent effects of amyloid precursor-like protein 2 in the SOD1-G37R transgenic mouse model of MND.Cellular and molecular life sciences : CMLS · 2021Article
- Conservative iron chelation for neurodegenerative diseases such as Parkinson's disease and amyotrophic lateral sclerosis.Journal of neural transmission (Vienna, Austria : 1996) · 2020Review
- The Prevalence of Insomnia and the Link between Iron Metabolism Genes Polymorphisms,International journal of environmental research and public health · 2020Article
- Phenotypic Effects of Wild-Type and Mutant SOD1 Expression in N9 Murine Microglia at Steady State, Inflammatory and Immunomodulatory Conditions.Frontiers in cellular neuroscience · 2019Article
- The Contribution of Iron to Protein Aggregation Disorders in the Central Nervous System.Frontiers in neuroscience · 2019Article
- Iron Metabolism of the Skeletal Muscle and Neurodegeneration.Frontiers in neuroscience · 2019Review
- Mitochondrial Targeting in Neurodegeneration: A Heme Perspective.Pharmaceuticals (Basel, Switzerland) · 2018Review
- Hepcidin, an emerging and important player in brain iron homeostasis.Journal of translational medicine · 2018Review
- Article
- New links between SOD1 and metabolic dysfunction from a yeast model of amyotrophic lateral sclerosis.Journal of cell science · 2016Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease characterized by degeneration and loss of motor neurons in the spinal cord, brainstem and motor cortex. Up to 10% of ALS cases are inherited (familial, fALS) and associated with mutations, frequently in the superoxide dismutase 1 (SOD1) gene. Rodent transgenic models of ALS are often used to elucidate a complex pathogenesis of this disease. Of importance, both ALS patients and animals carrying mutated human SOD1 gene show symptoms of oxidative stress and iron metabolism misregulation. The aim of our study was to characterize changes in iron metabolism in one of the most commonly used models of ALS - transgenic mice overexpressing human mutated SOD1(G93A) gene. We analyzed the expression of iron-related genes in asymptomatic, 2-month-old and symptomatic, 4-month-old SOD1(G93A) mice. In parallel, respective age-matched mice overexpressing human non-mutated SOD1 transgene and control mice were analyzed. We demonstrate that the overexpression of both SOD1 and SOD1(G93A) genes account for a substantial increase in SOD1 protein levels and activity in selected tissues and that not all the changes in iron metabolism genes expression are specific for the overexpression of the mutated form of SOD1.
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