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APOE modulates microglial immunometabolism in response to age, amyloid pathology, and inflammatory challenge [Bulk RNA-seq]

ABSTRACT: APOE modulates microglial immunometabolism in response to age, amyloid pathology, and inflammatory challenge [Bulk RNA-seq]

PROVIDER: PRJNA875087 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21350579_1.fastq.gz	Fastqsanger.gz
	SRR21350579_2.fastq.gz	Fastqsanger.gz
	SRR21350580_1.fastq.gz	Fastqsanger.gz
	SRR21350580_2.fastq.gz	Fastqsanger.gz
	SRR21350581_1.fastq.gz	Fastqsanger.gz

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APOE modulates microglial immunometabolism in response to age, amyloid pathology, and inflammatory challenge [Spatial transcriptomics]

Project description:The E4 allele of Apolipoprotein E (APOE) is associated with both metabolic dysfunction and a heightened pro-inflammatory response – two findings that may be intrinsically linked through the concept of immunometabolism. Here, we combined bulk, single-cell, and spatial transcriptomics with cell-specific and spatially resolved metabolic analyses to systematically address the role of APOE across age, neuroinflammation, and AD pathology. RNAseq highlighted immunometabolic changes across the APOE4 glial transcriptome, specifically in subsets of metabolically distinct microglia enriched in the E4 brain during aging or following an inflammatory challenge. E4 microglia display increased Hif1a expression, a disrupted TCA cycle, and are inherently pro-glycolytic, while spatial transcriptomics and MALDI mass spectrometry imaging highlight an E4-specific response to amyloid that is characterized by widespread alterations in lipid metabolism. Taken together, our findings emphasize a central role for APOE in regulating microglial immunometabolism.

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APOE modulates microglial immunometabolism in response to age, amyloid pathology, and inflammatory challenge [Bulk RNA-seq]

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APOE modulates microglial immunometabolism in response to age, amyloid pathology, and inflammatory challenge [scRNA-seq 1]

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APOE modulates microglial immunometabolism in response to age, amyloid pathology, and inflammatory challenge

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APOE modulates microglial immunometabolism in response to age, amyloid pathology, and inflammatory challenge [Spatial transcriptomics]

Project description:APOE modulates microglial immunometabolism in response to age, amyloid pathology, and inflammatory challenge [Spatial transcriptomics]

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APOE modulates microglial immunometabolism in response to age, amyloid pathology, and inflammatory challenge [scRNA-seq 1]

Project description:APOE modulates microglial immunometabolism in response to age, amyloid pathology, and inflammatory challenge [scRNA-seq 1]

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APOE modulates microglial immunometabolism in response to age, amyloid pathology, and inflammatory challenge.

Project description:The E4 allele of Apolipoprotein E (APOE) is associated with both metabolic dysfunction and a heightened pro-inflammatory response: two findings that may be intrinsically linked through the concept of immunometabolism. Here, we combined bulk, single-cell, and spatial transcriptomics with cell-specific and spatially resolved metabolic analyses in mice expressing human APOE to systematically address the role of APOE across age, neuroinflammation, and AD pathology. RNA sequencing (RNA-seq) highlighted immunometabolic changes across the APOE4 glial transcriptome, specifically in subsets of metabolically distinct microglia enriched in the E4 brain during aging or following an inflammatory challenge. E4 microglia display increased Hif1α expression and a disrupted tricarboxylic acid (TCA) cycle and are inherently pro-glycolytic, while spatial transcriptomics and mass spectrometry imaging highlight an E4-specific response to amyloid that is characterized by widespread alterations in lipid metabolism. Taken together, our findings emphasize a central role for APOE in regulating microglial immunometabolism and provide valuable, interactive resources for discovery and validation research.

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APOE modulates microglial immunometabolism in response to age, amyloid pathology, and inflammatory challenge

Project description:This SuperSeries is composed of the SubSeries listed below.

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APOE from astrocytes restores Alzheimer’s Aβ-pathology and DAM-like responses in APOE deficient microglia

Project description:The major genetic risk factor for Alzheimer’s disease (AD), APOE4, accelerates beta-amyloid (Aβ) plaque formation, but whether this is caused by APOE expressed in microglia or astrocytes is debated. We express here the human APOE isoforms in astrocytes in an Apoe-deficient AD mouse model. This is not only sufficient to restore the amyloid plaque pathology but also induces the characteristic transcriptional pathological responses in Apoe-deficient microglia surrounding the plaques. We find that both APOE4 and the protective APOE2 from astrocytes increase fibrillar plaque deposition, but differentially affect soluble Aβ aggregates. Microglia and astrocytes show specific alterations in function of APOE genotype expressed in astrocytes. Our experiments indicate a central role of the astrocytes in APOE mediated amyloid plaque pathology and in the induction of associated microglia responses.

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The VCAM1–ApoE pathway directs microglial chemotaxis and alleviates Alzheimer’s disease pathology

Project description:In Alzheimer’s disease (AD), sensome receptor dysfunction impairs microglial danger-associated molecular pattern (DAMP) clearance and exacerbates disease pathology. While extrinsic signals including interleukin-33 (IL-33) can restore microglial DAMP clearance, it remains largely unclear how the sensome receptor(s) is regulated and interacts with DAMP during phagocytic clearance. Here, we show that IL-33 induces VCAM1 in microglia, which promotes microglial chemotaxis toward amyloid-beta (Aβ) plaque-associated ApoE, and leads to Aβ clearance. We show that IL-33 stimulates a chemotactic state in microglia, characterized by Aβ-directed migration. Functional screening identified that VCAM1 directs microglial Aβ chemotaxis by sensing Aβ plaque-associated ApoE. Moreover, we found that disrupting VCAM1–ApoE interaction abolishes microglial Aβ chemotaxis, resulting in decreased microglial clearance of Aβ. In patients with AD, higher cerebrospinal fluid levels of soluble VCAM1 were correlated with impaired microglial Aβ chemotaxis. Together, our findings demonstrate that promoting VCAM1–ApoE-dependent microglial functions ameliorates AD pathology.

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