Evidence map›Paper›PMID 36051545›Full record

ArticleFrontiers in psychiatry2022

The relationship between TLR4/NF-κB/IL-1β signaling, cognitive impairment, and white-matter integrity in patients with stable chronic schizophrenia.

Hongna Li, Wenjin Chen, Mengzhuang Gou, Wei Li, Jinghui Tong, Yanfang Zhou, Ting Xie, Ting Yu, Wei Feng, Yanli Li and 12 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in psychiatry, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 2 pooled it
1.0field-weighted citation impact, top 30% 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

16 citing papers in PubMed, 2 syntheses or guidelines pooled it, 16 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
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

22 authors at 4 institutions in 3 countries.

Hongna LiPeking University HuiLongGuan Clinical Medical School, Beijing Huilongguan Hospital, Beijing, China.
Wenjin ChenPeking University HuiLongGuan Clinical Medical School, Beijing Huilongguan Hospital, Beijing, China.
Mengzhuang GouPeking University HuiLongGuan Clinical Medical School, Beijing Huilongguan Hospital, Beijing, China.
Wei LiPeking University HuiLongGuan Clinical Medical School, Beijing Huilongguan Hospital, Beijing, China.
Jinghui TongPeking University HuiLongGuan Clinical Medical School, Beijing Huilongguan Hospital, Beijing, China.
Yanfang ZhouPeking University HuiLongGuan Clinical Medical School, Beijing Huilongguan Hospital, Beijing, China.
Ting XiePeking University HuiLongGuan Clinical Medical School, Beijing Huilongguan Hospital, Beijing, China.
Ting YuPeking University HuiLongGuan Clinical Medical School, Beijing Huilongguan Hospital, Beijing, China.
Wei FengPeking University HuiLongGuan Clinical Medical School, Beijing Huilongguan Hospital, Beijing, China.
Yanli LiPeking University HuiLongGuan Clinical Medical School, Beijing Huilongguan Hospital, Beijing, China.
Song ChenPeking University HuiLongGuan Clinical Medical School, Beijing Huilongguan Hospital, Beijing, China.
Baopeng TianPeking University HuiLongGuan Clinical Medical School, Beijing Huilongguan Hospital, Beijing, China.
Shuping TanPeking University HuiLongGuan Clinical Medical School, Beijing Huilongguan Hospital, Beijing, China.
Zhiren WangPeking University HuiLongGuan Clinical Medical School, Beijing Huilongguan Hospital, Beijing, China.
Shujuan PanPeking University HuiLongGuan Clinical Medical School, Beijing Huilongguan Hospital, Beijing, China.
Na LiPeking University HuiLongGuan Clinical Medical School, Beijing Huilongguan Hospital, Beijing, China.
Xingguang LuoDepartment of Psychiatry, Yale University School of Medicine, New Haven, CT, United States.
Ping ZhangPeking University HuiLongGuan Clinical Medical School, Beijing Huilongguan Hospital, Beijing, China.
Junchao HuangPeking University HuiLongGuan Clinical Medical School, Beijing Huilongguan Hospital, Beijing, China.
Li TianDepartment of Physiology, Faculty of Medicine, Institute of Biomedicine and Translational Medicine, University of Tartu, Tartu, Estonia.
Chiang-Shan R LiDepartment of Psychiatry, Yale University School of Medicine, New Haven, CT, United States.
Yunlong TanPeking University HuiLongGuan Clinical Medical School, Beijing Huilongguan Hospital, Beijing, China.
Beijing HuiLongGuan Hospital · CNPeking University · CNYale University · USUniversity of Tartu · EE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objective: Previous studies have implicated intricate interactions between innate immunity and the brain in schizophrenia. Monocytic Toll-like receptor (TLR) 4 signaling, a crucial "sensor" of innate immunity, was reported to be over-activated in link with cognitive impairment in schizophrenia. As TLR4 is predominantly expressed on gliocytes prior to expression in neurons, we hypothesized that higher TLR4 levels may contribute to cognitive deterioration by affecting white matter microstructure. Methods: Forty-four patients with stable chronic schizophrenia (SCS) and 59 healthy controls (HCs) were recruited in this study. The monocytic function was detected with lipopolysaccharide (LPS) stimulation to simulate bacterial infection. Basal and LPS- stimulated levels of TLR4, nuclear factor-kappa B (NF-κB), and interleukin (IL)-1β were quantified with flow cytometry. Cognitive function was assessed by the MATRICS Consensus Cognitive Battery (MCCB) and psychopathological symptoms were evaluated by the Positive and Negative Syndrome Scale (PANSS). We employed diffusion tensor imaging with a 3-T scanner and evaluated white-matter integrity with fractional anisotropy (FA). Subcortical volume and cortical thickness were also assessed. Results: The TLR4/NF-κB/IL-1β signaling pathway was activated in patients with SCS, but responded sluggishly to LPS stimulation when compared with HCs. Furthermore, monocytic TLR4 expressions were inversely correlated with cognitive function and white matter FA, but not with cortical thickness or subcortical gray matter volume in schizophrenia. Conclusion: Our findings support altered TLR4 signaling pathway activity in association with deficits in cognition and white matter integrity in schizophrenia.

Indexed as

cognitioninflammationschizophreniaToll-like receptor 4white matter

Identifiers

PMID36051545
PMCPMC9424630
OpenAlexW4291824810

What OpenQuestion holds

Textmetadata
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.