Evidence map›Paper›PMID 28862638›Full record

ReviewThe Journal of clinical investigation2017

Microglia in Alzheimer's disease.

Heela Sarlus, Michael T Heneka

Abstract readReview
In one paragraph

Review in The Journal of clinical investigation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 538 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
538citing papers in PubMed, 5 pooled it
–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

538 citing papers in PubMed, 5 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. A Systematic Review of the Effects of Capsaicin on Alzheimer's Disease.International journal of molecular sciences · 2023
    Pooled it
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Increased circulating TREM2Brain, behavior, & immunity - health · 2026
    Article
  16. Neuroinflammation and Tauopathies.Molecular biology reports · 2026
    Review
  17. Review
  18. Article
  19. Article
  20. Article

478 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

2 authors.

Heela SarlusDepartment of Neurodegenerative Diseases and Gerontopsychiatry, University of Bonn, Bonn, Germany.
Michael T HenekaDepartment of Neurodegenerative Diseases and Gerontopsychiatry, University of Bonn, Bonn, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Microglia are brain-resident myeloid cells that mediate key functions to support the CNS. Microglia express a wide range of receptors that act as molecular sensors, which recognize exogenous or endogenous CNS insults and initiate an immune response. In addition to their classical immune cell function, microglia act as guardians of the brain by promoting phagocytic clearance and providing trophic support to ensure tissue repair and maintain cerebral homeostasis. Conditions associated with loss of homeostasis or tissue changes induce several dynamic microglial processes, including changes of cellular morphology, surface phenotype, secretory mediators, and proliferative responses (referred to as an "activated state"). Activated microglia represent a common pathological feature of several neurodegenerative diseases, including Alzheimer's disease (AD). Cumulative evidence suggests that microglial inflammatory activity in AD is increased while microglial-mediated clearance mechanisms are compromised. Microglia are perpetually engaged in a mutual interaction with the surrounding environment in CNS; thus, diverse microglial reactions at different disease stages may open new avenues for therapeutic intervention and modification of inflammatory activities. In this Review, the role of microglia in the pathogenesis of AD and the modulation of microglia activity as a therapeutic modality will be discussed.

Indexed as

Alzheimer DiseaseAnimalsBrainCell ProliferationCentral Nervous SystemComplement System ProteinsCytokinesHumansImmune SystemInflammationMacrophagesMiceMicrogliaNeurodegenerative DiseasesPhagocytosisToll-Like ReceptorsComplement System ProteinsCytokinesToll-Like Receptors

Identifiers

PMID28862638
PMCPMC5669553

What OpenQuestion holds

Textmetadata
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.