Evidence map›Paper›PMID 32588460›Full record

ReviewImmunological reviews2020

The role of innate immunity in Alzheimer's disease.

Hannah E Ennerfelt, John R Lukens

Open access · greenAbstract readReview
In one paragraph

Review in Immunological reviews, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed, 2 pooled it
7.2field-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

77 citing papers in PubMed, 2 syntheses or guidelines pooled it, 115 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Microglial CLEC7A restrains amyloid beta plaque pathology in a mouse model of Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  11. Review
  12. Article
  13. Article
  14. Nanoimmunomodulation of the Aβ-STING feedback machinery in microglia for Alzheimer's disease treatment.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  15. Review
  16. STING deletion protects against amyloid β-induced Alzheimer's disease pathogenesis.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  17. Review
  18. Review
  19. Rebalancing Immune Interactions within the Brain-Spleen Axis Mitigates Neuroinflammation in an Aging Mouse Model of Alzheimer's Disease.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025
    Article
  20. Review

17 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 at 1 institution in 1 country.

Hannah E EnnerfeltCenter for Brain Immunology and Glia (BIG), Department of Neuroscience, University of Virginia, Charlottesville, VA, USA.ORCID 0000-0003-4861-0740
John R LukensCenter for Brain Immunology and Glia (BIG), Department of Neuroscience, University of Virginia, Charlottesville, VA, USA.ORCID 0000-0002-6795-0866
University of Virginia · US

Funding

TRAINING IN CELL AND MOLECULAR BIOLOGYT32GM008136 · NIGMS · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI STUKENBERG, P. TODD · 1985 to 2020
$8.5M
Training in Cell and Molecular BiologyT32GM139787 · NIGMS · UNIVERSITY OF VIRGINIA · PI Bryce Paschal · 2021 to 2026
$2.5M
Inflammasome activation and lymphatic dysfunction in traumatic brain injuryR01NS106383 · NINDS · UNIVERSITY OF VIRGINIA · PI LUKENS, JOHN R · 2018 to 2022
$1.8M
NIGMS NIH HHS T32 GM008136NIGMS NIH HHS T32 GM139787NINDS NIH HHS R01 NS106383
6 · The paper itself

Abstract

The amyloid hypothesis has dominated Alzheimer's disease (AD) research for almost 30 years. This hypothesis hinges on the predominant clinical role of the amyloid beta (Aβ) peptide in propagating neurofibrillary tangles (NFTs) and eventual cognitive impairment in AD. Recent research in the AD field has identified the brain-resident macrophages, known as microglia, and their receptors as integral regulators of both the initiation and propagation of inflammation, Aβ accumulation, neuronal loss, and memory decline in AD. Emerging studies have also begun to reveal critical roles for distinct innate immune pathways in AD pathogenesis, which has led to great interest in harnessing the innate immune response as a therapeutic strategy to treat AD. In this review, we will highlight recent advancements in our understanding of innate immunity and inflammation in AD onset and progression. Additionally, there has been mounting evidence suggesting pivotal contributions of environmental factors and lifestyle choices in AD pathogenesis. Therefore, we will also discuss recent findings, suggesting that many of these AD risk factors influence AD progression via modulation of microglia and immune responses.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesBrainHumansImmunity, InnateMicrogliaAmyloid beta-PeptidesAlzheimer's diseaseamyloid betamicroglianeurodegenerative diseaseneuroimmunologyTREM2

Identifiers

PMID32588460
PMCPMC7783860
OpenAlexW3037473414

What OpenQuestion holds

Textmetadata
LicenceTDM
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.