Evidence map›Paper›PMID 31543810›Full record

ReviewFrontiers in aging neuroscience2019

Microglia in Alzheimer Disease: Well-Known Targets and New Opportunities.

Anne-Laure Hemonnot, Jennifer Hua, Lauriane Ulmann, Hélène Hirbec

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in aging neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 183 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
183citing papers in PubMed, 1 pooled it
22.2field-weighted citation impact, top 1% 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

183 citing papers in PubMed, 1 synthesis or guideline pooled it, 320 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. Review
  10. Gating mechanism of the two-pore-domain potassium channel THIK1.Nature structural & molecular biology · 2025
    Article
  11. Review
  12. Article
  13. Calcineurin inhibition may prevent Alzheimer disease in people with Down syndrome.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Review
  14. Article
  15. Review
  16. Review
  17. Review
  18. Article
  19. Review
  20. Article

123 more citing papers are in PubMed but not listed here.

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

4 authors at 1 institution in 1 country.

Anne-Laure HemonnotInstitute for Functional Genomics (IGF), University of Montpellier, Centre National de la Recherche Scientififique, Institut National de la Santé et de la Recherche Médicale, Montpellier, France.
Jennifer HuaInstitute for Functional Genomics (IGF), University of Montpellier, Centre National de la Recherche Scientififique, Institut National de la Santé et de la Recherche Médicale, Montpellier, France.
Lauriane UlmannInstitute for Functional Genomics (IGF), University of Montpellier, Centre National de la Recherche Scientififique, Institut National de la Santé et de la Recherche Médicale, Montpellier, France.
Hélène HirbecInstitute for Functional Genomics (IGF), University of Montpellier, Centre National de la Recherche Scientififique, Institut National de la Santé et de la Recherche Médicale, Montpellier, France.
Institut de Génomique Fonctionnelle · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Microglia are the resident macrophages of the central nervous system. They play key roles in brain development, and physiology during life and aging. Equipped with a variety of molecular sensors and through the various functions they can fulfill, they are critically involved in maintaining the brain's homeostasis. In Alzheimer disease (AD), microglia reaction was initially thought to be incidental and triggered by amyloid deposits and dystrophic neurites. However, recent genome-wide association studies have established that the majority of AD risk loci are found in or near genes that are highly and sometimes uniquely expressed in microglia. This leads to the concept of microglia being critically involved in the early steps of the disease and identified them as important potential therapeutic targets. Whether microglia reaction is beneficial, detrimental or both to AD progression is still unclear and the subject of intense debate. In this review, we are presenting a state-of-knowledge report intended to highlight the variety of microglial functions and pathways shown to be critically involved in AD progression. We first address both the acquisition of new functions and the alteration of their homeostatic roles by reactive microglia. Second, we propose a summary of new important parameters currently emerging in the field that need to be considered to identify relevant microglial targets. Finally, we discuss the many obstacles in designing efficient therapeutic strategies for AD and present innovative technologies that may foster our understanding of microglia roles in the pathology. Ultimately, this work aims to fly over various microglial functions to make a general and reliable report of the current knowledge regarding microglia's involvement in AD and of the new research opportunities in the field.

Indexed as

Alzheimer diseaseearly stagehiPSCsmicrogliamicroglia diversityneuroinflammationpurinergic signalingsexual dimorphism

Identifiers

PMID31543810
PMCPMC6730262
OpenAlexW2967683178

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.