Evidence map›Paper›PMID 36353359›Full record

ReviewFrontiers in molecular neuroscience2022

New insight into neurological degeneration: Inflammatory cytokines and blood-brain barrier.

Jie Yang, Mingzi Ran, Hongyu Li, Ye Lin, Kui Ma, Yuguang Yang, Xiaobing Fu, Siming Yang

Abstract readReview
In one paragraph

Review in Frontiers in molecular neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 178 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
178citing papers in PubMed, 4 pooled it
–field-weighted citation impact
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

178 citing papers in PubMed, 4 syntheses or guidelines pooled it.

  1. Pooled it
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  5. Review
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  7. The neuroimmune-glutamate hypothesis of addiction.Neuroscience and biobehavioral reviews · 2026
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118 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

8 authors.

Jie YangResearch Centre for Tissue Repair and Regeneration Affiliated to the Medical Innovation Research Department, PLA General Hospital, PLA Medical College, Beijing, China.
Mingzi RanResearch Centre for Tissue Repair and Regeneration Affiliated to the Medical Innovation Research Department, PLA General Hospital, PLA Medical College, Beijing, China.
Hongyu LiResearch Centre for Tissue Repair and Regeneration Affiliated to the Medical Innovation Research Department, PLA General Hospital, PLA Medical College, Beijing, China.
Ye LinDepartment of Neurology, The First Medical Centre, PLA General Hospital, Beijing, China.
Kui MaResearch Centre for Tissue Repair and Regeneration Affiliated to the Medical Innovation Research Department, PLA General Hospital, PLA Medical College, Beijing, China.
Yuguang YangDepartment of Dermatology, 4th Medical Centre, PLA General Hospital, Beijing, China.
Xiaobing FuResearch Centre for Tissue Repair and Regeneration Affiliated to the Medical Innovation Research Department, PLA General Hospital, PLA Medical College, Beijing, China.
Siming YangResearch Centre for Tissue Repair and Regeneration Affiliated to the Medical Innovation Research Department, PLA General Hospital, PLA Medical College, Beijing, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neurological degeneration after neuroinflammation, such as that resulting from Alzheimer's disease (AD), stroke, multiple sclerosis (MS), and post-traumatic brain injury (TBI), is typically associated with high mortality and morbidity and with permanent cognitive dysfunction, which places a heavy economic burden on families and society. Diagnosing and curing these diseases in their early stages remains a challenge for clinical investigation and treatment. Recent insight into the onset and progression of these diseases highlights the permeability of the blood-brain barrier (BBB). The primary factor that influences BBB structure and function is inflammation, especially the main cytokines including IL-1β, TNFα, and IL-6, the mechanism on the disruption of which are critical component of the aforementioned diseases. Surprisingly, the main cytokines from systematic inflammation can also induce as much worse as from neurological diseases or injuries do. In this review, we will therefore discuss the physiological structure of BBB, the main cytokines including IL-1β, TNFα, IL-6, and their mechanism on the disruption of BBB and recent research about the main cytokines from systematic inflammation inducing the disruption of BBB and cognitive impairment, and we will eventually discuss the need to prevent the disruption of BBB.

Indexed as

blood-brain barrierIL-1βIL-6inflammatory cytokinesneurological degenerationTNFα

Identifiers

PMID36353359
PMCPMC9637688

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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.