Evidence map›Paper›PMID 36942500›Full record

ArticleClinical science (London, England : 1979)2023

Neurochemical effects of sepsis on the brain.

Tatiana Barichello, Vijayasree V Giridharan, Carlos Henrique R Catalão, Cristiane Ritter, Felipe Dal-Pizzol

Open access · greenAbstract read
In one paragraph

Article in Clinical science (London, England : 1979), 2023. 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
3.3field-weighted citation impact, top 7% 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, 27 citations in OpenAlex.

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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

5 authors at 3 institutions in 2 countries.

Tatiana BarichelloFaillace Department of Psychiatry and Behavioral Sciences, McGovern Medical School, The University of Texas Health Science Center at Houston (UTHealth), Houston, TX, U.S.A.
Vijayasree V GiridharanFaillace Department of Psychiatry and Behavioral Sciences, McGovern Medical School, The University of Texas Health Science Center at Houston (UTHealth), Houston, TX, U.S.A.
Carlos Henrique R CatalãoFaillace Department of Psychiatry and Behavioral Sciences, McGovern Medical School, The University of Texas Health Science Center at Houston (UTHealth), Houston, TX, U.S.A.
Cristiane RitterGraduate Program in Health Sciences, Department of Medicine, University of Southern Santa Catarina (UNESC), Criciúma, SC, Brazil.
Felipe Dal-PizzolGraduate Program in Health Sciences, Department of Medicine, University of Southern Santa Catarina (UNESC), Criciúma, SC, Brazil.ORCID 0000-0003-3003-8977
Centro Universitário do Espírito Santo · BRThe University of Texas Health Science Center · USUniversidade de São Paulo · BR

Funding

Infection-driven mechanisms associated with Alzheimer's disease pathologyRF1AG072491 · NIA · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI BARICHELLO, TATIANA, MORALES, RODRIGO · 2021 to 2021
$2.0M
NIA NIH HHS RF1 AG072491
6 · The paper itself

Abstract

Sepsis is a life-threatening organ dysfunction triggered by a dysregulated host immune response to eliminate an infection. After the host immune response is activated, a complex, dynamic, and time-dependent process is triggered. This process promotes the production of inflammatory mediators, including acute-phase proteins, complement system proteins, cytokines, chemokines, and antimicrobial peptides, which are required to initiate an inflammatory environment for eliminating the invading pathogen. The physiological response of this sepsis-induced systemic inflammation can affect blood-brain barrier (BBB) function; subsequently, endothelial cells produce inflammatory mediators, including cytokines, chemokines, and matrix metalloproteinases (MMPs) that degrade tight junction (TJ) proteins and decrease BBB function. The resulting BBB permeability allows peripheral immune cells from the bloodstream to enter the brain, which then release a range of inflammatory mediators and activate glial cells. The activated microglia and astrocytes release reactive oxygen species (ROS), cytokines, chemokines, and neurochemicals, initiate mitochondrial dysfunction and neuronal damage, and exacerbate the inflammatory milieu in the brain. These changes trigger sepsis-associated encephalopathy (SAE), which has the potential to increase cognitive deterioration and susceptibility to cognitive decline later in life.

Indexed as

Endothelial CellsSepsisBlood-Brain BarrierBrainChemokinesCytokinesHumansInflammation MediatorsChemokinesCytokinesInflammation Mediatorsglial cellneuroinflammationsepsissepsis-associated encephalopathy

Identifiers

PMID36942500
PMCPMC11315270
OpenAlexW4328048361

What Socratic holds

Textmetadata
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 Socratic graph.