ArticleFrontiers in cellular neuroscience2022
Comprehensive expression analysis with cell-type-specific transcriptome in ALS-linked mutant SOD1 mice: Revisiting the active role of glial cells in disease.
Article in Frontiers in cellular neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 6 papers.
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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.
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- Microglial HVCN1 Deficiency Improves Movement and Survival of SOD1Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The Breakdown of Neurovascular Barriers: Molecular Mechanisms of Tight Junction Dysfunction.Molecular neurobiology · 2025Review
- Article
- Microglia in Neurodegenerative Diseases.Advances in neurobiology · 2024Review
- TDP-43 pathology in Drosophila induces glial-cell type specific toxicity that can be ameliorated by knock-down of SF2/SRSF1.PLoS genetics · 2023Article
- TDP-43 pathology inbioRxiv : the preprint server for biology · 2023Article
Corrections and comments
- Erratum issued
Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Non-cell autonomous mechanisms are involved in the pathogenesis of amyotrophic lateral sclerosis (ALS), an adult neurodegenerative disease characterized by selective motor neuron loss. While the emerging role of glial cells in ALS has been noted, the detailed cell-type-specific role of glial cells has not been clarified. Here, we examined mRNA expression changes using microarrays of the spinal cords of three distinct lines of mutant superoxide dismutase (SOD) 1 transgenic mice, an established ALS model. Our analysis used a transcriptome database of component cell types in the central nervous system (CNS), as well as SOD1
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