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ApoE expression marks microglial activation upon SCFA supplementation

ABSTRACT: ApoE expression marks microglial activation upon SCFA supplementation

PROVIDER: PRJNA705911 | ENA |

REPOSITORIES: ENA

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ApoE expression marks microglial activation upon SCFA supplementation

Project description:Transcriptomic Nanostring analysis from control and SCFA upplemented GF APPPS1 mice at 3 months of age

2021-03-03 | GSE168034 | GEO

Effect of individual SCFA on microglial polarization

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Effect of individual SCFA on microglial polarization

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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.

2023-07-18 | GSE208006 | GEO

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.

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SCFA

Project description:SCFA

| PRJNA705908 | ENA

Microglial-expressed Apoe does not modulate plaque pathogenesis

Project description:Microglial-expressed Apoe does not modulate plaque pathogenesis

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Microglial translational profiling reveals a convergent APOE pathway from aging, amyloid, and tau

Project description:Alzheimer’s disease (AD) is an age-associated neurodegenerative disease characterized by amyloidosis, tauopathy, and activation of microglia, the brain resident innate immune cells. We show that a RiboTag translational profiling approach can bypass biases due to cellular enrichment/cell sorting. In our recent study entitled “Microglial translational profiling reveals a convergent APOE pathway from aging, amyloid, and tau”, we utilized data acquired using this approach in models of amyloidosis, tauopathy, and aging, to reveal a common set of alterations and identified a central APOE-driven network that converged on CCL3 and CCL4 across all conditions. Notably, examination of the aged female dataset demonstrated a significant exacerbation of many of these shared transcripts in this APOE network, revealing a potential mechanism for increased AD susceptibility in females. This study has broad implications for microglial transcriptomic approaches and provides new insights into microglial pathways associated with different pathological aspects of aging and AD.

2018-07-25 | GSE117646 | GEO

Overexpressing low-density lipoprotein receptor reduces tau-associated neurodegeneration via apoE-dependent and independent mechanisms

Project description:APOE is the strongest genetic risk factor for late-onset Alzheimer’s disease. ApoE exacerbates tau-associated neurodegeneration by driving microglial activation. However, how apoE regulates microglial activation and whether targeting apoE is therapeutically beneficial in tauopathy is unclear. Here we show that overexpressing a low-density lipoprotein receptor (LDLR) transgene in P301S tau transgenic mice markedly reduces brain apoE and ameliorates tau pathology and neurodegeneration. ApoE specifically interacts with a high-molecular-weight tau species, and highly correlates with phospho-tau and insoluble tau levels. Microglial expression of the LDLR transgene reduces intracellular apoE and is associated with less microglial activation. snRNA-seq analysis of apoE-deficient or LDLR-overexpressing brains reveals that apoE deficiency drives microglial catabolism and increases the oligodendrocyte progenitor cell population. LDLR overexpression shares overlapping mechanisms, but uniquely upregulates microglial expression of specific ion channels and neurotransmitter receptors in tauopathy. A subset of disease-associated astrocytes with both neuroprotective and neurotoxic gene signatures is also identified.

2021-02-06 | GSE166261 | GEO

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Project description:The purpose of this study was to characterize the gene expression profile of MDA-MB-231 breast cancer cells treated with various SCFA-hexosamine analogs to better understand the role of various modifications to this scaffold. Keywords: SCFA-hexosamine analog comparison

2009-05-08 | GSE11407 | GEO

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