Evidence map›Paper›PMID 31134514›Full record

ArticleNeurochemical research2019

TREM2 Attenuates Aβ1-42-Mediated Neuroinflammation in BV-2 Cells by Downregulating TLR Signaling.

Huiping Long, Gang Zhong, Chengzhi Wang, Jian Zhang, Yueling Zhang, Jinglian Luo, Shengliang Shi

Erratum issuedAbstract read
PubMed Publisher
In one paragraph

Article in Neurochemical research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
2.8field-weighted citation impact, top 9% 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

33 citing papers in PubMed, 1 synthesis or guideline pooled it, 56 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Review
  6. Roles of TREM2 in Alzheimer's disease.Translational neurodegeneration · 2025
    Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. ERK1/2 in immune signalling.Biochemical Society transactions · 2022
    Review
  17. Review
  18. Glial Cell-Mediated Neuroinflammation in Alzheimer's Disease.International journal of molecular sciences · 2022
    Review
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Huiping LongDepartment of Neurology, The Second Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, China.
Gang ZhongGuangxi Medical University, Nanning, Guangxi, China.
Chengzhi WangDepartment of Neurology, The Third Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, China.
Jian ZhangDepartment of Neurology, The Second Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, China.
Yueling ZhangDepartment of Neurology, The Second Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, China.
Jinglian LuoDepartment of Neurology, The Second Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, China.
Shengliang ShiDepartment of Neurology, The Second Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, China. ssl_1964@163.com.
Guangxi Medical University · CN

Funding

Natural Science Foundation of China 81460183
6 · The paper itself

Abstract

The pathogenesis of late-onset Alzheimer's disease (LOAD) mainly involves abnormal accumulation of extracellular β-amyloid (Aβ) and the consequent neurotoxic effects. The triggering receptor expressed on myeloid cells 2 (TREM2) gene is associated with the pathogenesis of LOAD and plays important roles in mediating the phagocytosis of Aβ by microglia and regulating inflammation in central nervous system. However, the exact mechanisms of these processes have not yet been clarified. In this study, we investigated the mechanism by which TREM2 regulates neuroinflammation and promotes Aβ1-42 clearance by BV-2 cells and further elucidated the underlying molecular mechanisms. We either silenced or overexpressed TREM2 in BV-2 cells and evaluated the cell viability, Aβ1-42 content, and expression of inflammatory markers (IL-1β, IL-6, and TNF-α). TREM2 overexpression up-regulated cell activity, promoted clearance of Aβ1-42 by BV-2 cells, and down-regulated expression of the inflammatory factors. In addition, TREM2 overexpression downregulation the expression of the TLR family (TLR2, TLR4 and TLR6) in BV-2 cells. Moreover, LPS, as an agonist of the TLR family, up-regulated the expression of inflammatory cytokines (IL-1β, TNF-α, and IL-6) in BV-2 cells overexpressing TREM2. In conclusion, TREM2 promoted clearance of Aβ1-42 by BV-2 cells and restored BV-2 cell viability from Aβ1-42-mediated neuroinflammation by downregulating TLRs. These findings suggest that TREM2 may be a target for LOAD therapy.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsCell Line, TransformedCell SurvivalDown-RegulationInflammationInterleukin-1betaInterleukin-6Membrane GlycoproteinsMicePeptide FragmentsPhagocytosisReceptors, ImmunologicSignal TransductionToll-Like ReceptorsAmyloid beta-Peptidesamyloid beta-protein (1-42)IL1B protein, mouseInterleukin-1betaInterleukin-6interleukin-6, mouseMembrane GlycoproteinsPeptide FragmentsReceptors, ImmunologicToll-Like ReceptorsTrem2 protein, mouseTumor Necrosis Factor-alphaAlzheimer's diseaseNeuroinflammationTLR signalingTREM2

Identifiers

PMID31134514
OpenAlexW2947065666

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Registered trials

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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.