Evidence map›Paper›PMID 27395435›Full record

ReviewBrain, behavior, and immunity2017

Inflammation in Alzheimer's disease: Lessons learned from microglia-depletion models.

Elizabeth E Spangenberg, Kim N Green

Abstract readReview
In one paragraph

Review in Brain, behavior, and immunity, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 186 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
186citing papers in PubMed, 2 pooled it
13.8field-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

186 citing papers in PubMed, 2 syntheses or guidelines pooled it, 362 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Article
  5. Inflammation profiles in Alzheimer's disease relate to cognition and neurodegeneration.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  6. Review
  7. Neuroprotective effects ofBiomedical reports · 2026
    Article
  8. The evolving landscape of amyloid-targeting therapies in Alzheimer's disease: progress and challenges.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026
    Review
  9. Review
  10. Utilizing nanotechnology to diagnose and treat central nervous system disorders.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026
    Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Myeloperoxidase as a therapeutic target for oxidative damage in Alzheimer's disease.Journal of enzyme inhibition and medicinal chemistry · 2025
    Review
  17. Article
  18. Microglial plasticity across development mediates infantile amnesia.bioRxiv : the preprint server for biology · 2025
    Article
  19. Review
  20. Review

126 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.

Elizabeth E SpangenbergDepartment of Neurobiology and Behavior, Institute for Memory Impairments and Neurological Disorders, United States.
Kim N GreenDepartment of Neurobiology and Behavior, Institute for Memory Impairments and Neurological Disorders, United States. Electronic address: kngreen@uci.edu.
Institute of Neurobiology · BG

Funding

UC Irvine Alzheimer's Disease Research Center Induced Pluripotent Stem Cell CoreP50AG016573 · NIA · UNIVERSITY OF CALIFORNIA-IRVINE · PI LAFERLA, FRANK M · 2000 to 2019
$37.0M
Origins, properties, and therapeutic potential of cells that repopulate the microglia-depleted adult brainR01NS083801 · NINDS · UNIVERSITY OF CALIFORNIA-IRVINE · PI Kim Green · 2014 to 2026
$5.6M
NIA NIH HHS P50 AG016573NINDS NIH HHS R01 NS083801
6 · The paper itself

Abstract

Microglia are the primary immune cell of the brain and function to protect the central nervous system (CNS) from injury and invading pathogens. In the homeostatic brain, microglia serve to support neuronal health through synaptic pruning, promoting normal brain connectivity and development, and through release of neurotrophic factors, providing support for CNS integrity. However, recent evidence indicates that the homeostatic functioning of these cells is lost in neurodegenerative disease, including Alzheimer's disease (AD), ultimately contributing to a chronic neuroinflammatory environment in the brain. Importantly, the development of compounds and genetic models to ablate the microglial compartment has emerged as effective tools to further our understanding of microglial function in AD. Use of these models has identified roles of microglia in several pathological facets of AD, including tau propagation, synaptic stripping, neuronal loss, and cognitive decline. Although culminating evidence utilizing these microglial ablation models reports an absence of CNS-endogenous and peripheral myeloid cell involvement in Aβ phagocytosis, recent data indicates that targeting microglia-evoked neuroinflammation in AD may be essential for potential therapeutics. Therefore, identifying altered signaling pathways in the microglia-devoid brain may assist with the development of effective inflammation-based therapies in AD.

Indexed as

Alzheimer DiseaseAnimalsBrainDisease Models, AnimalInflammationMicrogliaNeuronsPhagocytosistau Proteinstau ProteinsAlzheimer’s diseaseAmyloidColony-stimulating factor 1 receptorInflammationMicrogliaSpinesTau

Identifiers

PMID27395435
PMCPMC5218993
OpenAlexW2460405435

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.