Evidence map›Paper›PMID 31182681›Full record

ArticleAging2019

Kainic acid Induces production and aggregation of amyloid β-protein and memory deficits by activating inflammasomes in NLRP3- and NF-κB-stimulated pathways.

Yang Ruan, Xiang Qiu, Yu-Dan Lv, Dong Dong, Xiu-Juan Wu, Jie Zhu, Xiang-Yu Zheng

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Aging, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.8field-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

24 citing papers in PubMed, 39 citations in OpenAlex.

  1. Review
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  9. Article
  10. Article
  11. Article
  12. Inflammasomes in neurodegenerative diseases.Translational neurodegeneration · 2024
    Review
  13. Therapeutic targeting of senescent cells in the CNS.Nature reviews. Drug discovery · 2024
    Review
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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

7 authors at 3 institutions in 2 countries.

Yang RuanKey Laboratory of Pathobiology, Ministry of Education, College of Basic Medical Sciences, Jilin University, Changchun 130021, China.
Xiang QiuDepartment of Radiology, The First Hospital of Jilin University, Changchun 130021, China.
Yu-Dan LvDepartment of Neurology and Neuroscience Center, The First Hospital of Jilin University, Changchun 130021, China.
Dong DongDepartment of Radiology, The First Hospital of Jilin University, Changchun 130021, China.
Xiu-Juan WuDepartment of Neurology and Neuroscience Center, The First Hospital of Jilin University, Changchun 130021, China.
Jie ZhuDepartment of Neurology and Neuroscience Center, The First Hospital of Jilin University, Changchun 130021, China.
Xiang-Yu ZhengDepartment of Neurology and Neuroscience Center, The First Hospital of Jilin University, Changchun 130021, China.
First Hospital of Jilin University · CNJilin University · CNKarolinska Institutet · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Kainic acid (KA) treatment causes neuronal degeneration, which is a feature of Alzheimer's disease (AD) symptoms such as amyloid β-protein production and memory deficits. Inflammasomes are known to be critical for the progression of AD. However, the underlying mechanism by which inflammasomes influence AD progression remains unknown. The present study investigated the damaging effect of KA on neurons by focusing on the inflammasome-mediated signaling pathways. Assessments using cultured microglia and mouse brains demonstrated that KA treatment specifically induced inflammasome activation. Mechanistic evaluations showed that KA activated two major components of inflammasomes, nucleotide binding oligomerization domain (NOD)-like receptor (NLR) protein 3 (NLRP3) and nuclear factor (NF)-κB, which resulted in the production of interleukin-1β (IL-1β) and brain-derived neurotrophic factor (BDNF). Inhibition of NLRP3 or NF-κB by Bay11-7082 caused a reduction in the KA-induced expression of interleukin (IL)-1β and BDNF. Moreover, knockdown of the expression of KA receptors (KARs) such as Grik1 and Grik3 induced suppression of NLRP3 and NF-κB, suggesting that KARs function upstream of NLRP3 and NF-κB to mediate the effects of KA on regulation of IL-1β and BDNF expression. Notably, IL-1β was shown to exert positive effects on the expression of BACE1, which is blocked by Bay11-7082. Overall, our results revealed that Bay11-7082 acts against KA-induced neuronal degeneration, amyloid β-protein (Aβ) deposition, and memory defects via inflammasomes and further highlighted the protective role of Bay11-7082 in KA-induced neuronal defects.

Indexed as

Amyloid beta-PeptidesAnimalsInflammasomesKainic AcidMemory DisordersMiceMicrogliaNeuronsNF-kappa BNLR Family, Pyrin Domain-Containing 3 ProteinProtein AggregatesReactive Oxygen SpeciesSignal TransductionAmyloid beta-PeptidesInflammasomesKainic AcidNF-kappa BNLR Family, Pyrin Domain-Containing 3 ProteinProtein AggregatesReactive Oxygen Speciesbrain-derived neurotrophic factorinterleukin-1βkainic acidNF-κBNLRP3

Identifiers

PMID31182681
PMCPMC6594814
OpenAlexW2951706708

What OpenQuestion holds

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LicenceCC BY
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.