ArticleActa neuropathologica communications2024
Deciphering glial contributions to CSF1R-related disorder via single-nuclear transcriptomic profiling: a case study.
Article in Acta neuropathologica communications, 2024. 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 11 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.
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.
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Who cites it
11 citing papers in PubMed.
- Correction to: Deciphering glial contributions to CSF1R-related disorder via single-nuclear transcriptomic profiling: a case study.Acta neuropathologica communications · 2026Article
- Long-term clinical and biomarker observations following rituximab exposure in two siblings with CSF1R-related leukoencephalopathy: a preliminary familial case series.Communications medicine · 2026Article
- CX3CL1/CX3CR1-dependent microglial phagocytosis of oligodendrocyte precursor cells contributes to sevoflurane-induced myelination impairments in neonatal mice.Journal of neuroinflammation · 2026Article
- Disruption of CSF-1 receptor-mediated metal ion homeostasis in the murine brain promotes neurodegenerative disease.The Journal of clinical investigation · 2026Article
- A strategy of microglia replacement alleviates microgliopathy in a CSF1R I794T hotspot mutation mouse model of CSF1R-related disorder.Cell reports. Medicine · 2026Article
- Microglial handling of myelin debris and remyelination after ischaemic stroke: recognition, intracellular processing, lipid fate, and oligodendroglial repair.Frontiers in cellular neuroscience · 2026Review
- Diversity and function of tumor-associated macrophages in brain metastases: mechanisms and therapeutic prospects.Frontiers in immunology · 2026Review
- CSF1R-related leukoencephalopathy presenting with early apathy, hypoactivity, and cognitive flattening: a case report of a diagnostic challenge.Frontiers in human neuroscience · 2026Article
- Dynamic Intercellular Networks in the CNS: Mechanisms of Crosstalk from Homeostasis to Neurodegeneration.International journal of molecular sciences · 2025Review
- Mutations in the human CSF1R gene impact microglia's maintenance of brain white matter integrity.Nature immunology · 2025Article
- Editorial: Immune therapies in neurological disorders.Frontiers in neuroscience · 2025Article
Corrections and comments
- Erratum issued
Authors and funding
10 authors.
Funding
Abstract
CSF1R-related disorder (CSF1R-RD) is a neurodegenerative condition that predominantly affects white matter due to genetic alterations in the CSF1R gene, which is expressed by microglia. We studied an elderly man with a hereditary, progressive dementing disorder of unclear etiology. Standard genetic testing for leukodystrophy and other neurodegenerative conditions was negative. Brain autopsy revealed classic features of adult-onset leukoencephalopathy with axonal spheroids and pigmented glia (ALSP), including confluent white matter degeneration with axonal spheroids and pigmented glial cells in the affected white matter, consistent with CSF1R-RD. Subsequent long-read sequencing identified a novel deletion in CSF1R that was not detectable with short-read exome sequencing. To gain insight into potential mechanisms underlying white matter degeneration in CSF1R-RD, we studied multiple brain regions exhibiting varying degrees of white matter pathology. We found decreased CSF1R transcript and protein across brain regions, including intact white matter. Single nuclear RNA sequencing (snRNAseq) identified two disease-associated microglial cell states: lipid-laden microglia (expressing GPNMB, ATG7, LGALS1, LGALS3) and inflammatory microglia (expressing IL2RA, ATP2C1, FCGBP, VSIR, SESN3), along with a small population of CD44
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