Evidence map›Paper›PMID 39218898›Full record

ArticleJournal of neuroinflammation2024

Microglia either promote or restrain TRAIL-mediated excitotoxicity caused by Aβ

Jian Zou, Elizabeth McNair, Sagan DeCastro, Scott P Lyons, Angie Mordant, Laura E Herring, Ryan P Vetreno, Leon G Coleman

Abstract read
In one paragraph

Article in Journal of neuroinflammation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

9 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Loss of lysosomal acid lipase contributes to Alzheimer's disease pathology and cognitive decline.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  9. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors.

Jian ZouBowles Center for Alcohol Studies, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC, 27599, USA.
Elizabeth McNairBowles Center for Alcohol Studies, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC, 27599, USA.
Sagan DeCastroBowles Center for Alcohol Studies, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC, 27599, USA.
Scott P LyonsDepartment of Pharmacology, UNC Proteomics Core, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC, 27599, USA.
Angie MordantDepartment of Pharmacology, UNC Proteomics Core, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC, 27599, USA.
Laura E HerringDepartment of Pharmacology, UNC Proteomics Core, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC, 27599, USA.
Ryan P VetrenoBowles Center for Alcohol Studies, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC, 27599, USA.
Leon G ColemanBowles Center for Alcohol Studies, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC, 27599, USA. leon_coleman@med.unc.edu.

Funding

Virology Research Program (Program 4)P30CA016086 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Deborah F. Tate · 1985 to 2026
$201.5M
Microglia Activation and TLR-induced Neurodegeneration by Alcohol Promotes Progression of Alzheimer PathologyR01AA028924 · NIAAA · UNIV OF NORTH CAROLINA CHAPEL HILL · PI COLEMAN, LEON GARLAND, CREWS, FULTON T · 2020 to 2024
$1.9M
Adolescent Alcohol in 5xFAD Mouse Model Accelerates Neuroinflammation and Alzheimer's Disease Pathology Across AgingR01AG072894 · NIA · UNIV OF NORTH CAROLINA CHAPEL HILL · PI VETRENO, RYAN PETER · 2020 to 2024
$1.9M
NIAAA NIH HHS R01 AA028924NIA NIH HHS R01 AG072894NIH HHS AA028924NIH HHS AG072894NIH HHS CA016086
6 · The paper itself

Abstract

backgroundAlzheimer's disease (AD) features progressive neurodegeneration and microglial activation that results in dementia and cognitive decline. The release of soluble amyloid (Aβ) oligomers into the extracellular space is an early feature of AD pathology. This can promote excitotoxicity and microglial activation. Microglia can adopt several activation states with various functional outcomes. Protective microglial activation states have been identified in response to Aβ plaque pathology in vivo. However, the role of microglia and immune mediators in neurotoxicity induced by soluble Aβ oligomers is unclear. Further, there remains a need to identify druggable molecular targets that promote protective microglial states to slow or prevent the progression of AD.

methodsHippocampal entorhinal brain slice culture (HEBSC) was employed to study mechanisms of Aβ

resultsNeurotoxicity induced by soluble Aβ

conclusionMicroglia are key mediators of both protection and neurodegeneration in response to Aβ. Polarizing microglia toward a protective state could be used as a preventative strategy against Aβ-induced neurotoxicity.

Indexed as

Amyloid beta-PeptidesMicrogliaPeptide FragmentsTNF-Related Apoptosis-Inducing LigandAnimalsEntorhinal CortexHippocampusMiceMice, Inbred C57BLOrgan Culture TechniquesAmyloid beta-Peptidesamyloid beta-protein (1-42)Peptide FragmentsTNF-Related Apoptosis-Inducing LigandAlzheimer’s diseaseAmyloidMicrogliaNeurodegenerationTRAIL

Identifiers

PMID39218898
PMCPMC11367981

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.