Evidence map›Paper›PMID 31693761›Full record

ArticleJournal of neurochemistry2020

Iron potentiates microglial interleukin-1β secretion induced by amyloid-β.

Israel C Nnah, Chih-Hao Lee, Marianne Wessling-Resnick

Open access · greenAbstract read
In one paragraph

Article in Journal of neurochemistry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

40 citing papers in PubMed, 47 citations in OpenAlex.

  1. Review
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  4. Acidosis, Iron Dyshomeostasis and Inflammatory Injury.International journal of molecular sciences · 2026
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  8. SS-31 improves post-cardiac arrest brain injury by inhibiting microglial ferroptosis and polarization.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
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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

3 authors at 1 institution in 1 country.

Israel C NnahDepartment of Molecular Metabolism, Harvard TH Chan School of Public Health, Boston, MA, USA.
Chih-Hao LeeDepartment of Molecular Metabolism, Harvard TH Chan School of Public Health, Boston, MA, USA.ORCID 0000-0002-6090-0786
Marianne Wessling-ResnickDepartment of Molecular Metabolism, Harvard TH Chan School of Public Health, Boston, MA, USA.ORCID 0000-0002-7919-1633
Harvard University · US

Funding

Microgial Iron Metabolism and Its Regulation by CannabinoidsR01DK064750 · NIDDK · HARVARD UNIVERSITY (SCH OF PUBLIC HLTH) · PI LEE, CHIH-HAO · 2004 to 2021
$4.2M
Interdisciplinary Training in Genes and the EnvironmentT32ES016645 · NIEHS · HARVARD SCHOOL OF PUBLIC HEALTH · PI LEE, CHIH-HAO · 2008 to 2018
$4.0M
NIDDK NIH HHS R01 DK064750NIEHS NIH HHS T32 ES016645
6 · The paper itself

Abstract

Alzheimer's disease (AD) is characterized by accumulation of amyloid-beta (Aβ) senile plaques in patients' brain tissues. Elevated levels of interleukin-1beta (IL-1β) have been identified in cerebrospinal fluid of living AD patients and in animal models of AD. Increased expression of IL-1β and iron accumulation have been identified in microglial cells that cluster around amyloid plaques in AD mouse models and post-mortem brain tissues of AD patients. The goals of this study were to determine the effects of Aβ on the secretion of IL-1β by microglial cells and whether iron status influences this pro-inflammatory signaling cue. Immortalized microglial (IMG) cells were incubated with Aβ with or without iron. qRT-PCR and western blot analyses showed that Aβ induces biosynthesis of IL-1β by IMG cells. IMG cells secrete the mature form of IL-1β in a caspase 1-dependent manner. Incubation with iron provoked a greater pro-inflammatory response. Inhibition of the iron transporter divalent metal transporter 1 protected IMG cells against Aβ-induced inflammation. Potentiation of Aβ-elicited IL-1β induction by iron was also antagonized by ROS inhibitors, supporting the model that divalent metal transporter 1-mediated iron loading and subsequent increase in ROS contribute to the inflammatory effects of Aβ in microglia. Immunoblotting and immunofluorescence microscopy indicate that iron enhances Aβ activation of NF-κB signaling to promote IL-1β synthesis. These results support the hypothesis that Aβ stimulates IL-1β expression by activating NF-κB signaling in microglia cells. Most importantly, iron appears to exacerbate the pro-inflammatory effects of Aβ to increase IL-1β levels.

Indexed as

Amyloid beta-PeptidesAnimalsCell LineInterleukin-1betaIronMiceMicrogliaAmyloid beta-PeptidesInterleukin-1betaIronAlzheimer’s diseasedivalent metal transporter-1IMG (immortalized microglia) cellsironmicroglianeuroinflammation

Identifiers

PMID31693761
PMCPMC7565447
OpenAlexW2986676869

What OpenQuestion holds

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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.