ArticleJournal of neuroinflammation2013
Dysregulation of the complement cascade in the hSOD1G93A transgenic mouse model of amyotrophic lateral sclerosis.
Article in Journal of neuroinflammation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02869048 (Amyotrophic Lateral Sclerosis and the Innate Immune System), which is not on this map. Cited by 57 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.
Amyotrophic Lateral Sclerosis and the Innate Immune System
Who cites it
57 citing papers in PubMed, 94 citations in OpenAlex.
- Efficacy and Safety of Ravulizumab, a Complement C5 Inhibitor, in Adults With Amyotrophic Lateral Sclerosis: A Randomized Clinical Trial.JAMA neurology · 2023Trial
- Safety and Feasibility of Lin- Cells Administration to ALS Patients: A Novel View on Humoral Factors and miRNA Profiles.International journal of molecular sciences · 2018Trial
- Role of complement and complement-targeted therapeutics in neurological diseases.Nature reviews. Neurology · 2026Review
- Site-targeted proximal complement C3 inhibition, but not C5 blockade, attenuates neurodegeneration in a mouse model of amyotrophic lateral sclerosis: Implications for failed clinical trials.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Article
- Size-dependent alterations in phrenic motor neuron perineuronal nets following cervical spinal hemisection.Journal of neurophysiology · 2026Article
- The evidence for old age motor neuron death: A scoping review.Physiological reports · 2026Article
- Aspirin Attenuates the Pathogenesis of Amyotrophic Lateral Sclerosis by Inhibiting the Activities of Microglia in a NF-κB-dependent Complement System-deactivating Mechanism.Molecular neurobiology · 2025Article
- A Comparative Analysis of Grip Strength Evaluation Methods in a Large Cohort of Aged Mice.Journal of cachexia, sarcopenia and muscle · 2025Article
- Review
- Lymphatic dysfunction correlates with inflammation in a mouse model of amyotrophic lateral sclerosis.Disease models & mechanisms · 2025Article
- Overexpression of the schizophrenia risk gene C4 in PV cells drives sex-dependent behavioral deficits and circuit dysfunction.iScience · 2024Article
- C5aR1 antagonism suppresses inflammatory glial responses and alters cellular signaling in an Alzheimer's disease mouse model.Nature communications · 2024Article
- Overexpression of the schizophrenia risk gene C4 in PV cells drives sex-dependent behavioral deficits and circuit dysfunction.bioRxiv : the preprint server for biology · 2024Article
- Timeline of hypoglossal motor neuron death and intrinsic tongue muscle denervation in high-copy number SOD1Frontiers in neurology · 2024Article
- Microglial Metabolic Reprogramming: Emerging Insights and Therapeutic Strategies in Neurodegenerative Diseases.Cellular and molecular neurobiology · 2023Review
- The Complement System in the Central Nervous System: From Neurodevelopment to Neurodegeneration.Biomolecules · 2022Review
- The emerging role of complement in neuromuscular disorders.Seminars in immunopathology · 2021Review
- Adjuvant Lineage-Negative Cell Therapy as a Potential Silencer of the Complement-Mediated Immune System in ALS Patients.Journal of clinical medicine · 2021Article
- Interplay between immunity and amyotrophic lateral sclerosis: Clinical impact.Neuroscience and biobehavioral reviews · 2021Review
- A Novel Diagnostic Predictive Model for Idiopathic Short Stature in Children.Frontiers in endocrinology · 2021Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundComponents of the innate immune complement system have been implicated in the pathogenesis of amyotrophic lateral sclerosis (ALS); however, a comprehensive examination of complement expression in this disease has not been performed. This study therefore aimed to determine the expression of complement components (C1qB, C4, factor B, C3/C3b, C5 and CD88) and regulators (CD55 and CD59a) in the lumbar spinal cord of hSOD1(G93A) mice during defined disease stages.
methodshSOD1(G93A) and wild-type mice were examined at four different ages of disease progression. mRNA and protein expression of complement components and regulators were examined using quantitative PCR, western blotting and ELISA. Localisation of complement components within lumbar spinal cord was investigated using immunohistochemistry. Statistical differences between hSOD1(G93A) and wild-type mice were analysed using a two-tailed t-test at each stage of disease progression.
resultsWe found several early complement factors increased as disease progressed, whilst complement regulators decreased; suggesting overall increased complement activation through the classical or alternative pathways in hSOD1(G93A) mice. CD88 was also increased during disease progression, with immunolocalisation demonstrating expression on motor neurons and increasing expression on microglia surrounding the regions of motor neuron death.
conclusionsThese results indicate that local complement activation and increased expression of CD88 may contribute to motor neuron death and ALS pathology in the hSOD1(G93A) mouse. Hence, reducing complement-induced inflammation could be an important therapeutic strategy to treat ALS.
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Registered trials
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