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Alzheimer’s disease-induced phagocytic microglia express a specific profile of coding and non-coding RNAs [short RNA]

ABSTRACT: To detect miRNAs in microglia derived from AD mice (5xFAD) brain we single cell sorted Cd11b+ and Cd45+ cells divided by Methoxy-X04 staining (Ab aggregates) positivity We performed differentially expression analysis of RNA-seq of wild-type microglia (Me-X04 neg), non-phagocytic AD microglia (Me-X04 neg), phagocytic AD microglia (Me-X04 positive)

ORGANISM(S): Mus musculus

PROVIDER: GSE229417 | GEO | 2024/03/20

REPOSITORIES: GEO

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Alzheimer’s disease-induced phagocytic microglia express a specific profile of coding and non-coding RNAs [lncRNA]

Project description:To detect total RNA in microglia derived from AD mice (5xFAD) brain we single cell sorted Cd11b+ and Cd45+ cells divided by Methoxy-X04 staining (Ab aggregates) positivity We performed differentially expression analysis of RNA-seq of wild-type microglia (Me-X04 neg), non-phagocytic AD microglia (Me-X04 neg), phagocytic AD microglia (Me-X04 positive)

2024-03-20 | GSE229418 | GEO

The microglial transcriptome of a novel murine model of Alzheimer's Disease: phagocytically active and inactive microglia from homozygous App-SAA mice and WT littermate controls.

Project description:We created a novel murine model of Alzheimer's Disease using a knock-in strategy to humanize the sequence of the murine App gene and introduced three familial AD (FAD) mutations, Swedish (Swedish (KM670/671NL), Arctic (E693G)) and Austrian (T712I). To determine whether App-SAA microglia exhibit cellular dysfunctions and whether these dysfunctions relate to fibrillar Ab internalization, mice were intraperitoneally (i.p.) injected with 10 mg/kg methoxy-X04. 24 hours after injection, mice were perfused with PBS, cortical and hippocampal tissues were dissected and processed into single-cell suspension and methoxy-X04-negative and methoxy-X04-positive microglia were isolated using FACS. Mirroring our gene expression studies, we found profound alterations of the AppSAA microglia transcriptome; these changes were exacerbated in methoxy-X04 positive compared to negative cells.

2021-01-20 | GSE158153 | GEO

Alzheimer’s disease-induced phagocytic microglia express a specific profile of coding and non-coding RNAs

Project description:Alzheimer’s disease-induced phagocytic microglia express a specific profile of coding and non-coding RNAs

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TREM2 regulates microglial cholesterol metabolism upon chronic phagocytic challenge [bulk RNA-seq]

Project description:TREM2 is a microglial-specific gene implicated in late-onset Alzheimer's Disease (AD). Recent studies have identified that Trem2-deficient mice exhibit transcriptional changes in microglial gene expression that minimize the upregulation of lipid metabolism and lysosomal genes in AD disease models. We find that chronic phagocytic challenge from demyelination generates similiarly attenuated expression of lysosomal and lipid metabolism genes in microglia isolated from Trem2 knockout mouse brain.

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TREM2 regulates microglial cholesterol metabolism upon chronic phagocytic challenge [single-cell RNA-Seq]

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Alzheimer’s disease-induced phagocytic microglia express a specific profile of coding and non-coding RNAs [lncRNA]

Project description:Alzheimer’s disease-induced phagocytic microglia express a specific profile of coding and non-coding RNAs [lncRNA]

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Gene expression profile of phagocytic and non-phagocytic microglia following traumatic brain injury and nasal anti-CD3 treatment

Project description:Bulk RNA-sequencing was performed to investigate the transcriptomic signature of phagocytic and non-phagocytic microglia following traumatic brain injury and nasal anti-CD3 treatment.

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Alzheimer’s disease-induced phagocytic microglia express a specific profile of coding and non-coding RNAs [short RNA]

Project description:Alzheimer’s disease-induced phagocytic microglia express a specific profile of coding and non-coding RNAs [short RNA]

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Transcriptome profiling of phagocytic or non-phagocytic microglia from Ifngr1 cKO mice.

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Naturally-aged microglia exhibit phagocytic dysfunction accompanied by gene expression changes reflective of underlying neurologic disease

Project description:Age-associated microglial dysfunction contributes to the accumulation of amyloid-b (Ab) plaques in Alzheimer’s disease. Although several studies have shown age-related declines in the phagocytic capacity of myeloid cells, relatively few have examined phagocytosis of normally aged microglia. Furthermore, much of the existing data on aging microglial function have been generated in accelerated genetic models of Alzheimer’s disease. Here we found that naturally aged microglia phagocytosed less Ab over time. To gain a better understanding of such dysfunction, we assessed differences in gene expression between young and old microglia that either did or did not phagocytose Ab. Young microglia had both phagocytic and neuronal maintenance signatures indicative of normal microglial responses, whereas, old microglia, regardless of phagocytic status, exhibit signs of broad dysfunction reflective of underlying neurologic disease states. We also found downregulation of many phagocytic receptors on old microglia, including TREM2, an Ab phagocytic receptor. TREM2 protein expression was diminished in old microglia and loss of TREM2+ microglia was correlated with impaired Ab uptake, suggesting a mechanism for phagocytic dysfunction in old microglia. Combined, our work reveals that normally aged microglia have broad changes in gene expression, including defects in Ab phagocytosis that likely underlies the progression to neurologic disease.

2022-06-10 | GSE205803 | GEO

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