ArticleGlia2026
Altered Inflammatory Signature in a C9ORF72 -ALS iPSC-Derived Motor Neuron and Microglia Coculture Model.
Article in Glia, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed.
- Lysosomal dysfunction in neurodegenerative disease.Nature reviews. Neurology · 2026Review
- Microglia in C9orf72-associated amyotrophic lateral sclerosis: More or less active?Neural regeneration research · 2026Article
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Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Amyotrophic lateral sclerosis (ALS) is a complex neurodegenerative disorder involving multiple cell types in the central nervous system. The key pathological features of ALS include the degeneration of motor neurons and the initiation and propagation of neuroinflammation mediated by nonneuronal cell types such as microglia. Currently, the specific mechanisms underlying the involvement of microglia in neuroinflammation in ALS are unclear. Consequently, we generated several human-induced pluripotent stem cell (iPSC) derived motor neuron and microglia cocultures. We utilized ALS patient-derived iPSCs carrying a common genetic variant, the hexanucleotide repeat expansion (HRE) in C9ORF72, as well as C9ORF72 knockout (KO) iPSC lines. iPSC-derived motor neurons and microglia demonstrated expression of cell type-specific markers and were functional. Phenotypic assessments on motor neurons and microglia in mono- and cocultures identified dysfunction in the expression and secretion of inflammatory cytokines and chemokines in lipopolysaccharide (LPS)-stimulated C9ORF72 HRE and C9ORF72 KO microglia. Analysis of single-cell RNA sequencing data from microglia and motor neuron cocultures revealed cell type-specific transcriptomic changes. Specifically, we detected the removal of an LPS-responsive microglia subpopulation, correlating with a dampened inflammatory response in C9ORF72 HRE and C9ORF72 KO microglia. Overall, our results support the critical role of microglia-mediated neuroinflammation in ALS pathology, and our iPSC-derived models should prove a valuable platform for further mechanistic studies of ALS-associated pathways.
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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 Socratic graph.