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Sustained microglial depletion with CSF1R inhibitor impairs parenchymal plaque development in an Alzheimer’s disease model

ABSTRACT: This dataset allows for the exploration of microglial function on gene expression in wild-type and the 5xFAD mouse model of Alzheimer's disease, across multiple brain regions. Mice were treated with the selective CSF1R inhibitor PLX5622, which eliminates >95% of microglia in less than 5 days, from 1.5 to 7 months of age. Thus, these data allow the exploration of the effects, and specificity, of 6 months microglial depletion, in both wild-type and 5xFAD mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE134151 | GEO | 2019/07/12

REPOSITORIES: GEO

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single-cell RNA-seq profile of adult microglia under acute Csf1r inhibition and early repopulation

Project description:Microglia are the resident myeloid cell in the central nervous system (CNS). Like other terminally differentiated myeloid cells, microglia rely on Csf1r signaling for survival and maintenance. Surprisingly, a small subset of microglia in the murine brain can survive without Csf1r signaling, as shown in Csf1r KO mice as well as in mice that have been treated with Csf1r inhibitor PLX5622. The nature of such Csf1r independent microglial population has not been fully characterized. Here we applied single-cell RNA-seq to examine the remaining microglia in C57/BL6J mice that were treated with PLX5622 diet (1200 mg/kg, 14 days), which results >90% microglial removal.

2019-12-01 | GSE133773 | GEO

single-cell RNA-seq profile of microglia under acute Csf1r inhibition and early repopulation in adult brain

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Microglial-expressed Apoe does not modulate plaque pathogenesis

Project description:This dataset allows for the exploration of the effect of microglial-expressed Apoe knockout in a 5xFAD Alzheimer's Disease model.

2021-10-15 | GSE185622 | GEO

Sustained microglial depletion with CSF1R inhibitor impairs parenchymal plaque development in an Alzheimer’s disease model

Project description:Sustained microglial depletion with CSF1R inhibitor impairs parenchymal plaque development in an Alzheimer’s disease model

| PRJNA554106 | ENA

Sustained microglial depletion with CSF1R inhibitor impairs parenchymal plaque development in an Alzheimer's disease model.

Project description: Not available

| S-EPMC6704256 | biostudies-literature

CSF1R inhibition by PLX5622 affects multiple immune cell compartments with tissue-specific metabolic effects

Project description:We found that long-term CSF1R-inhibition by PLX5622 depleted tissue resident macrophages in different organs. This alteration resulted in a dual impact on glucose homeostasis with improved insulin sensitivity predominantly in the liver, combined with an insulin secretion defect in the islets of Langerhans. RNA-Seq analysis of islets of mice treated with PLX5622 compared to control mice hinted at a role of IL-1β in supporting insulin secretion,

2023-06-29 | GSE189434 | GEO

Gene expression of macrophages isolated from mouse brains

Project description:Hematogenous macrophages infiltrate the brain after virus infection. We use a CSF1R inhibitior, PLX5622 to deplete microglia from the brain. However, macrophages also express the CSF1R and may be affected by PLX5622-treatment of mice.

2018-02-28 | GSE103379 | GEO

The CSF1R-Microglia Axis Has Protective Host-Specific Roles During Neurotropic Picornavirus Infection

Project description:Goal: Determine the role of microglia in the antiviral response during neurotropic picornavirus infection of C57BL/6J and SJL/J mice and whether absence of microglia would affect CD4 and CD8 T cell functions. Methods: Brains from C57BL/6J and SJL/J mice treated with PLX5622 (to deplete microlgia) or control diet were harvested at 6 days post TMEV-infection. CD4+ T cells and CD8+ T cells were obtained using Easy Sep Mouse CD4+ T cell isolation Kit and Easy Sep Mouse CD8+ T cell isolation Kit (Stemcell). RNA was obtained using RNeasy (QIAGEN) and Illumina TruSeq stranded RNA Kit with Ribo-Zero Gold was then utilized to prepare cDNA library for RNA-seq. Results: Our results demonstrate strain-specific effects of the CSF1R-microglia axis in the context of neurotropic viral infection as well as inherent differences in microglial antigen presentation and subsequent T cell crosstalk that contribute to susceptibility to neurotropic picornavirus infection.

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Engineering an inhibitor resistant human CSF1R variant for microglia replacement [InVivo_RNA]

Project description:iPSC-derived hematopoietic progenitor cells expressing either the wildtype or G795A CSF1R variant were xenotransplanted into neonatal mice and subsequently aged for two months to compare in vivo gene expression differences between the two CSF1R genotypes.

2022-12-21 | GSE220214 | GEO

Therapeutic potential of human microglial transplantation in a chimeric model of CSF1R-related leukoencephalopathy

Project description:Adult-onset leukoencephalopathy with axonal spheroids and pigmented glia (ALSP) is a rare, autosomal dominant primary microgliopathy caused by mutations in colony-stimulating factor 1 receptor (CSF1R). CSF1R signaling is necessary for microglial differentiation and survival. As a result, ALSP patient brains have fewer microglia and exhibit an array of neuropathologies including axonal spheroids, white matter abnormalities, reactive astrocytosis, and brain calcification. To explore the therapeutic potential of transplanting healthy human microglia, we generated ‘hFIRE’ mice, a xenotolerant mouse model of ALSP that lacks murine microglia. Remarkably, transplantation of induced pluripotent stem cell (iPSC)-derived microglial progenitors enabled rapid CNS-wide microglial engraftment, restoring a homeostatic microglial gene signature and preventing diverse ALSP-related neuropathologies. To further examine a potential autologous approach, ALSP-patient derived iPSCs were CRISPR-corrected, rescuing mutation-induced deficits in microglial proliferation, enabling brain-wide microglial engraftment, and reducing pre-existing spheroid, astroglial, and calcification pathologies within just 6 weeks. Together with the accompanying study by Munro and Colleagues, these results demonstrate the utility of FIRE mice to model diverse ALSP neuropathologies and provide initial evidence that iPSC-microglia could be further developed as a promising new therapeutic strategy for ALSP and perhaps other microglia-associated neurological disorders.

2024-04-24 | GSE253623 | GEO

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