ArticleProceedings of the National Academy of Sciences of the United States of America2007
Toxicity from different SOD1 mutants dysregulates the complement system and the neuronal regenerative response in ALS motor neurons.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. 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 81 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
81 citing papers in PubMed, 141 citations in OpenAlex.
- Activating Transcription Factor 3 in Pain: A Molecular Regulator and Emerging Biomarker.Genes · 2026Review
- Reevaluating the role of beta2-microglobulin: new insights on selective vulnerability in ALS pathology.Acta neuropathologica · 2026Article
- Excitotoxicity in amyotrophic lateral sclerosis: a key pathogenic mechanism.Brain communications · 2026Review
- Transcriptional modulation unique to vulnerable motor neurons predicts ALS across species and SOD1 mutations.Genome research · 2025Article
- ALS/FTD-linked TBK1 deficiency in microglia induces an aged-like microglial signature and drives social recognition deficits in mice.Nature communications · 2025Article
- Complex Genetic Framework in Familial Amyotrophic Lateral Sclerosis With a C9ORF72 Mutation: A Case Report.Cureus · 2024Article
- Astrocyte-Neuron Interactions Contributing to Amyotrophic Lateral Sclerosis Progression.Advances in neurobiology · 2024Review
- Involvement of Lipids in the Pathogenesis of Amyotrophic Lateral Sclerosis.Life (Basel, Switzerland) · 2023Review
- SPY1 inhibits neuronal ferroptosis in amyotrophic lateral sclerosis by reducing lipid peroxidation through regulation of GCH1 and TFR1.Cell death and differentiation · 2023Article
- Long-term effects of l-serine supplementation upon a mouse model of diabetic neuropathy.Journal of diabetes and its complications · 2023Article
- Immunology of amyotrophic lateral sclerosis - role of the innate and adaptive immunity.Frontiers in neuroscience · 2023Review
- Impaired disassembly of the axon initial segment restricts mitochondrial entry into damaged axons.The EMBO journal · 2022Article
- Anti-Inflammatory Effects of GLP-1 Receptor Activation in the Brain in Neurodegenerative Diseases.International journal of molecular sciences · 2022Review
- α-Amino-3-hydroxyl-5-methyl-4-isoxazole-propionate receptor and RNA processing gene dysregulation are early determinants of selective motor neuron vulnerability in a mouse model of amyotrophic lateral sclerosis.Brain communications · 2022Article
- Translatomic analysis of regenerating and degenerating spinal motor neurons in injury and ALS.iScience · 2021Article
- Sporadic Amyotrophic Lateral Sclerosis Due to a FUS P525L Mutation with Asymmetric Muscle Weakness and Anti-ganglioside Antibodies.Internal medicine (Tokyo, Japan) · 2021Article
- Aberrant Complement System Activation in Neurological Disorders.International journal of molecular sciences · 2021Review
- Sterol auto-oxidation adversely affects human motor neuron viability and is a neuropathological feature of amyotrophic lateral sclerosis.Scientific reports · 2021Article
- Complement Profiles in Patients with Amyotrophic Lateral Sclerosis: A Prospective Observational Cohort Study.Journal of inflammation research · 2021Article
- The good, the bad, and the opportunities of the complement system in neurodegenerative disease.Journal of neuroinflammation · 2020Review
21 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
3 authors at 1 institution in 1 country.
Funding
Abstract
Global, age-dependent changes in gene expression from rodent models of inherited ALS caused by dominant mutations in superoxide-dismutase 1 (SOD1) were identified by using gene arrays and RNAs isolated from purified embryonic and adult motor neurons. Comparison of embryonic motor neurons expressing a dismutase active ALS-linked mutant SOD1 with those expressing comparable levels of wild-type SOD1 revealed the absence of mutant-induced mRNA changes. An age-dependent mRNA change that developed presymptomatically in adult motor neurons collected by laser microdissection from mice expressing dismutase active ALS-linked mutants was dysregulation of the d/l-serine biosynthetic pathway, previously linked to both excitotoxic and neurotrophic effects. An unexpected dysregulation common to motor neurons expressing either dismutase active or inactive mutants was induction of neuronally derived components of the classic complement system and the regenerative/injury response. Alteration of these mutant SOD1-induced pathways identified a set of targets for therapies for inherited ALS.
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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.