Evidence map›Paper›PMID 36376530›Full record

ArticleScientific reports2022

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

Alyssa L Thomas, Maria A Lehn, Edith M Janssen, David A Hildeman, Claire A Chougnet

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
6.7field-weighted citation impact, top 2% of its field
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

58 citing papers in PubMed, 84 citations in OpenAlex.

  1. miR-214-3p and NCKAP1: A microglial functional dimension of Alzheimer's progression.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  2. Review
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  6. Microglia extract neuronal proteolytic organelles via skoupocytosis.bioRxiv : the preprint server for biology · 2026
    Article
  7. Review
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  17. Review
  18. Microglial phagocytosis in Alzheimer disease.Nature reviews. Neurology · 2026
    Review
  19. Review
  20. Article
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

5 authors at 2 institutions in 1 country.

Alyssa L ThomasDepartment of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH, USA.
Maria A LehnImmunology Graduate Program, Cincinnati Children's Hospital Medical Center and the University of Cincinnati College of Medicine, Cincinnati, OH, USA.
Edith M JanssenImmunology Graduate Program, Cincinnati Children's Hospital Medical Center and the University of Cincinnati College of Medicine, Cincinnati, OH, USA.
David A HildemanDepartment of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH, USA. david.hildeman@cchmc.org.
Claire A ChougnetDepartment of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH, USA. Claire.Chougnet@cchmc.org.
Cincinnati Children's Hospital Medical Center · USUniversity of Cincinnati · US

Funding

Tissue Repository CoreP30AR070549 · NIAMS · CINCINNATI CHILDRENS HOSP MED CTR · PI Grant Sanford Schulert · 2016 to 2026
$7.7M
Homeostasis and function of regulatory T cells in agingR01AG033057 · NIA · CINCINNATI CHILDRENS HOSP MED CTR · PI CHOUGNET, CLAIRE A., HILDEMAN, DAVID A · 2009 to 2018
$3.5M
Metabolic alterations in age-associated dendritic cell dysfunctionR01AG053498 · NIA · CINCINNATI CHILDRENS HOSP MED CTR · PI CHOUGNET, CLAIRE A., HILDEMAN, DAVID A · 2017 to 2021
$2.9M
Homeostasis and function of regulatory T cells in agingR56AG033057 · NIA · CINCINNATI CHILDRENS HOSP MED CTR · PI CHOUGNET, CLAIRE A., HILDEMAN, DAVID A · 2019 to 2019
$643k
Regulation and function of immune suppressive T cells in agingR56AG065327 · NIA · CINCINNATI CHILDRENS HOSP MED CTR · PI CHOUGNET, CLAIRE A., HILDEMAN, DAVID A · 2021 to 2021
$326k
NIAMS NIH HHS P30 AR070549NIA NIH HHS R01 AG033057NIA NIH HHS R01 AG053498NIA NIH HHS R56 AG033057NIA NIH HHS R56 AG065327
6 · The paper itself

Abstract

Age-associated microglial dysfunction contributes to the accumulation of amyloid-β (Aβ) 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 Aβ 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 Aβ. 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 Aβ phagocytic receptor. TREM2 protein expression was diminished in old microglia and loss of TREM2

Indexed as

Alzheimer DiseaseMicrogliaAmyloid beta-PeptidesAnimalsDisease Models, AnimalGene ExpressionPhagocytosisPlaque, AmyloidAmyloid beta-Peptides

Identifiers

PMID36376530
PMCPMC9663419
OpenAlexW4308968236

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.