Evidence map›Paper›PMID 35488237›Full record

ReviewJournal of neuroinflammation2022

Sepsis-associated brain injury: underlying mechanisms and potential therapeutic strategies for acute and long-term cognitive impairments.

Nobufumi Sekino, Magdy Selim, Amjad Shehadah

Abstract readReview
In one paragraph

Review in Journal of neuroinflammation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed, 2 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

70 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Article
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  5. Article
  6. Article
  7. Observational
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Potentiating Cerebral Perfusion Normalizes Glymphatic Dynamics in Systemic Inflammation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Sepsis in patients with severe TBI: a retrospective CT scoring study.International journal of emergency medicine · 2025
    Article
  20. Review

10 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

3 authors.

Nobufumi SekinoDepartment of Medicine, Translational Therapeutics Division, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, 02215, USA.
Magdy SelimDepartment of Neurology, Stroke and Cerebrovascular Diseases Division, Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brookline Avenue, CLS-641, Boston, MA, 02215, USA.
Amjad ShehadahDepartment of Neurology, Stroke and Cerebrovascular Diseases Division, Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brookline Avenue, CLS-641, Boston, MA, 02215, USA. ashehada@bidmc.harvard.edu.

Funding

Role of Tau Conformations in Vascular Contribution to Cognitive Impairment and DementiaR01AG055559 · NIA · BETH ISRAEL DEACONESS MEDICAL CENTER · PI LO, ENG H., SHEHADAH, AMJAD · 2017 to 2021
$3.4M
NIA NIH HHS R01 AG055559
6 · The paper itself

Abstract

Sepsis is a life-threatening organ dysfunction caused by a dysregulated host response to infection. Sepsis causes cerebral dysfunction in the short and long term and induces disruption of the blood-brain barrier (BBB), neuroinflammation, hypoperfusion, and accumulation of amyloid β (Aβ) and tau protein in the brain. White matter changes and brain atrophy can be detected using brain imaging, but unfortunately, there is no specific treatment that directly addresses the underlying mechanisms of cognitive impairments in sepsis. Here, we review the underlying mechanisms of sepsis-associated brain injury, with a focus on BBB dysfunction and Aβ and tau protein accumulation in the brain. We also describe the neurological manifestations and imaging findings of sepsis-associated brain injury, and finally, we propose potential therapeutic strategies for acute and long-term cognitive impairments associated with sepsis. In the acute phase of sepsis, we suggest using antibiotics (such as rifampicin), targeting proinflammatory cytokines, and preventing ischemic injuries and hypoperfusion. In the late phase of sepsis, we suggest targeting neuroinflammation, BBB dysfunction, Aβ and tau protein phosphorylation, glycogen synthase kinase-3 beta (GSK3β), and the receptor for advanced glycation end products (RAGE). These proposed strategies are meant to bring new mechanism-based directions for future basic and clinical research aimed at preventing or ameliorating acute and long-term cognitive impairments in patients with sepsis.

Indexed as

Brain InjuriesCognitive DysfunctionSepsisAmyloid beta-PeptidesHumanstau ProteinsAmyloid beta-Peptidestau ProteinsAlzheimer’s diseaseAmyloid-betaCognitive impairmentNeuroinflammationSepsisTau proteinWhite matter change

Identifiers

PMID35488237
PMCPMC9051822

What OpenQuestion holds

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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.