Summary of Study ST002451

This data is available at the NIH Common Fund's National Metabolomics Data Repository (NMDR) website, the Metabolomics Workbench, https://www.metabolomicsworkbench.org, where it has been assigned Project ID PR001580. The data can be accessed directly via it's Project DOI: 10.21228/M8G711 This work is supported by NIH grant, U2C- DK119886.

See: https://www.metabolomicsworkbench.org/about/howtocite.php

This study contains a large results data set and is not available in the mwTab file. It is only available for download via FTP as data file(s) here.

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Study IDST002451
Study TitleAPOE modulates microglial immunometabolism in response to age, amyloid pathology, and inflammatory challenge (Part 2 of 3)
Study SummaryThe 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 Hif1α 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.
Institute
University of Kentucky
DepartmentPhysiology
LaboratoryLance Johnson; Josh Morganti
Last NameDevanney
First NameNicholas
AddressPhysiology, 760 Press Ave, Healthy Kentucky Research Bldg, Rm152, Lexington, Kentucky, 40508, USA
EmailNicholas.Devanney@uky.edu
Phone8593238083
Submit Date2023-01-20
Study CommentsPart 2 of 3
Raw Data AvailableYes
Raw Data File Type(s)cdf
Analysis Type DetailGC-MS
Release Date2023-01-25
Release Version1
Nicholas Devanney Nicholas Devanney
https://dx.doi.org/10.21228/M8G711
ftp://www.metabolomicsworkbench.org/Studies/ application/zip

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Factors:

Subject type: Mammal; Subject species: Mus musculus (Factor headings shown in green)

mb_sample_id local_sample_id Group APOE genotype Treatment
SA24505847_3_12E3_control E3/E3 Control
SA24505947_3_1E3_control E3/E3 Control
SA24506047_3_11E3_control E3/E3 Control
SA24506147_3_10E3_control E3/E3 Control
SA24506247_3_2E3_control E3/E3 Control
SA24506347_3_4E3_control E3/E3 Control
SA24506447_3_3E3_control E3/E3 Control
SA24506547_3_9E3_control E3/E3 Control
SA24506647_3_14E3_proinflammatory E3/E3 Proinflammatory
SA24506747_3_15E3_proinflammatory E3/E3 Proinflammatory
SA24506847_3_13E3_proinflammatory E3/E3 Proinflammatory
SA24506947_3_16E3_proinflammatory E3/E3 Proinflammatory
SA24507047_3_8E3_proinflammatory E3/E3 Proinflammatory
SA24507147_3_5E3_proinflammatory E3/E3 Proinflammatory
SA24507247_3_6E3_proinflammatory E3/E3 Proinflammatory
SA24507347_3_7E3_proinflammatory E3/E3 Proinflammatory
SA24507447_4_12E4_control E4/E4 Control
SA24507547_4_9E4_control E4/E4 Control
SA24507647_4_10E4_control E4/E4 Control
SA24507747_4_4E4_control E4/E4 Control
SA24507847_4_2E4_control E4/E4 Control
SA24507947_4_1E4_control E4/E4 Control
SA24508047_4_3E4_control E4/E4 Control
SA24508147_4_15E4_proinflammatory E4/E4 Proinflammatory
SA24508247_4_16E4_proinflammatory E4/E4 Proinflammatory
SA24508347_4_14E4_proinflammatory E4/E4 Proinflammatory
SA24508447_4_8E4_proinflammatory E4/E4 Proinflammatory
SA24508547_4_6E4_proinflammatory E4/E4 Proinflammatory
SA24508647_4_7E4_proinflammatory E4/E4 Proinflammatory
SA24508747_4_13E4_proinflammatory E4/E4 Proinflammatory
Showing results 1 to 30 of 30
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