Evidence map›Paper›PMID 35232622›Full record

ReviewSeminars in immunology2022

APOE mediated neuroinflammation and neurodegeneration in Alzheimer's disease.

Samira Parhizkar, David M Holtzman

Open access · hybridAbstract readReview
In one paragraph

Review in Seminars in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 159 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
159citing papers in PubMed, 1 pooled it
17.2field-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

159 citing papers in PubMed, 1 synthesis or guideline pooled it, 220 citations in OpenAlex.

  1. Pooled it
  2. Brain, behavior, & immunity - health · 2026
    Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Mechanisms, Biomarkers and Therapeutic Implications of Neuroinflammation in Alzheimer's Disease.International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience · 2026
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Journal of Korean medical science · 2026
    Article
  14. Review
  15. Article
  16. Review
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  19. Review
  20. Article

99 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.

Samira ParhizkarDepartment of Neurology, Hope Center for Neurological Disorders, Knight Alzheimer Disease, Research Center, Washington University, St. Louis, MO, 63110, USA.
David M HoltzmanDepartment of Neurology, Hope Center for Neurological Disorders, Knight Alzheimer Disease, Research Center, Washington University, St. Louis, MO, 63110, USA. Electronic address: holtzman@wustl.edu.
Hope Center for Neurological Disorders · US

Funding

Project 4 (Genetic modifiers for APOE-associated Alzheimer's disease pathogenesis)U19AG069701 · NIA · MAYO CLINIC JACKSONVILLE · PI Celeste Marie Karch · 2021 to 2026
$42.0M
Effect of APOE on CNS Neurons: Role of LRPRF1NS090934 · NINDS · WASHINGTON UNIVERSITY · PI HOLTZMAN, DAVID M. · 2020 to 2025
$6.5M
Novel Strategies and Mechanisms to Target APOE and Alzheimer's DiseaseRF1AG047644 · NIA · WASHINGTON UNIVERSITY · PI HOLTZMAN, DAVID M., HYMAN, BRADLEY T. · 2019 to 2019
$3.8M
NIA NIH HHS RF1 AG047644NIA NIH HHS U19 AG069701NINDS NIH HHS RF1 NS090934
6 · The paper itself

Abstract

Neuroinflammation is a central mechanism involved in neurodegeneration as observed in Alzheimer's disease (AD), the most prevalent form of neurodegenerative disease. Apolipoprotein E4 (APOE4), the strongest genetic risk factor for AD, directly influences disease onset and progression by interacting with the major pathological hallmarks of AD including amyloid-β plaques, neurofibrillary tau tangles, as well as neuroinflammation. Microglia and astrocytes, the two major immune cells in the brain, exist in an immune-vigilant state providing immunological defense as well as housekeeping functions that promote neuronal well-being. It is becoming increasingly evident that under disease conditions, these immune cells become progressively dysfunctional in regulating metabolic and immunoregulatory pathways, thereby promoting chronic inflammation-induced neurodegeneration. Here, we review and discuss how APOE and specifically APOE4 directly influences amyloid-β and tau pathology, and disrupts microglial as well as astroglial immunomodulating functions leading to chronic inflammation that contributes to neurodegeneration in AD.

Indexed as

Alzheimer DiseaseNeurodegenerative DiseasesApolipoprotein E4HumansInflammationNeuroinflammatory DiseasesApolipoprotein E4Alzheimer’s diseaseApolipoprotein EAstrocytesInflammationMicrogliaNeurodegeneration

Identifiers

PMID35232622
PMCPMC9411266
OpenAlexW4214714809

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.