Evidence map›Paper›PMID 33450391›Full record

ArticleNeurobiology of disease2021

Analysis of homozygous and heterozygous Csf1r knockout in the rat as a model for understanding microglial function in brain development and the impacts of human CSF1R mutations.

Omkar L Patkar, Melanie Caruso, Ngari Teakle, Sahar Keshvari, Stephen J Bush, Clare Pridans, Arnauld Belmer, Kim M Summers, Katharine M Irvine, David A Hume

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neurobiology of disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
5.6field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

33 citing papers in PubMed, 70 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 6 institutions in 2 countries.

Omkar L PatkarMater Research Institute-University of Queensland, Translational Research Institute, Brisbane, Queensland, Australia.
Melanie CarusoMater Research Institute-University of Queensland, Translational Research Institute, Brisbane, Queensland, Australia.
Ngari TeakleMater Research Institute-University of Queensland, Translational Research Institute, Brisbane, Queensland, Australia.
Sahar KeshvariMater Research Institute-University of Queensland, Translational Research Institute, Brisbane, Queensland, Australia.
Stephen J BushNuffield Department of Clinical Medicine, John Radcliffe Hospital, University of Oxford, Oxford, UK.
Clare PridansUniversity of Edinburgh Centre for Inflammation Research, Edinburgh, UK and Simons Initiative for the Developing Brain, Centre for Discovery Brain Sciences, University of Edinburgh, UK.
Arnauld BelmerSchool of Clinical Sciences, Queensland University of Technology, Brisbane, Australia.
Kim M SummersMater Research Institute-University of Queensland, Translational Research Institute, Brisbane, Queensland, Australia.
Katharine M IrvineMater Research Institute-University of Queensland, Translational Research Institute, Brisbane, Queensland, Australia.
David A HumeMater Research Institute-University of Queensland, Translational Research Institute, Brisbane, Queensland, Australia. Electronic address: David.Hume@uq.edu.au.
Translational Research Institute · AUUniversity of Queensland · AUJohn Radcliffe Hospital · GBMater Research · AUQueensland University of Technology · AUUniversity of Edinburgh · GB

Funding

Medical Research Council MR/M019969/1
6 · The paper itself

Abstract

Mutations in the human CSF1R gene have been associated with dominant and recessive forms of neurodegenerative disease. Here we describe the impacts of Csf1r mutation in the rat on development of the brain. Diffusion imaging indicated small reductions in major fiber tracts that may be associated in part with ventricular enlargement. RNA-seq profiling revealed a set of 105 microglial markers depleted in all brain regions of the Csf1rko rats. There was no evidence of region or sex-specific expression of microglia-associated transcripts. Other than the microglial signature, Csf1rko had no effect on any neuronal or region-specific transcript cluster. Expression of markers of oligodendrocytes, astrocytes, dopaminergic neurons and Purkinje cells was minimally affected. However, there were defects in dendritic arborization of doublecortin-positive neurogenic precursors and expression of poly-sialylated neural cell adhesion molecule (PS-NCAM) in the dentate gyrus of the hippocampus. Heterozygous Csf1rko rats had no detectable brain phenotype. We conclude that most brain developmental processes occur normally in the absence of microglia and that CSF1R haploinsufficiency is unlikely to cause leukoencephalopathy.

Indexed as

MicrogliaAnimalsDisease Models, AnimalFemaleGene Knockout TechniquesHumansMaleMutationNeurodegenerative DiseasesNeurogenesisRatsReceptor, Macrophage Colony-Stimulating FactorReceptors, Granulocyte-Macrophage Colony-Stimulating FactorCSF1R protein, humanReceptor, Macrophage Colony-Stimulating FactorReceptors, Granulocyte-Macrophage Colony-Stimulating FactorCSF1RHippocampusKnockoutLeukoencephalopathyMicrogliaNeurogenicRatRNA-seq

Identifiers

PMID33450391
PMCPMC7941205
OpenAlexW3118602645

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.