Evidence map›Paper›PMID 28588507›Full record

ReviewFrontiers in psychiatry2017

Neurovascular Unit Dysfunction and Blood-Brain Barrier Hyperpermeability Contribute to Schizophrenia Neurobiology: A Theoretical Integration of Clinical and Experimental Evidence.

Souhel Najjar, Silky Pahlajani, Virginia De Sanctis, Joel N H Stern, Amanda Najjar, Derek Chong

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in psychiatry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 126 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
126citing papers in PubMed, 3 pooled it
7.3field-weighted citation impact, top 2% 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

126 citing papers in PubMed, 3 syntheses or guidelines pooled it, 213 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Article
  5. Review
  6. Review
  7. Article
  8. Neuronal genetic risk within the multicellular landscape of schizophrenia.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
    Article
  9. Article
  10. Article
  11. Article
  12. The role of tight junction proteins in the pathogenesis of schizophrenia.European archives of psychiatry and clinical neuroscience · 2026
    Review
  13. Article
  14. Review
  15. Article
  16. Review
  17. Spatially resolved translational dysregulation inbioRxiv : the preprint server for biology · 2025
    Article
  18. Review
  19. Article
  20. Review

66 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

6 authors at 3 institutions in 1 country.

Souhel NajjarDepartment of Neurology, Hofstra Northwell School of Medicine, New York, NY, USA.
Silky PahlajaniNeuroinflammation Division, Department of Neurology, Lenox Hill Hospital, New York, NY, USA.
Virginia De SanctisNeuroinflammation Division, Department of Neurology, Lenox Hill Hospital, New York, NY, USA.
Joel N H SternDepartment of Neurology, Hofstra Northwell School of Medicine, New York, NY, USA.
Amanda NajjarDepartment of Psychology and Human Development, Peabody College, Vanderbilt University, Nashville, TN, USA.
Derek ChongDepartment of Neurology, Hofstra Northwell School of Medicine, New York, NY, USA.
Hofstra University · USLenox Hill Hospital · USVanderbilt University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Schizophrenia is a psychotic disorder characterized by delusions, hallucinations, negative symptoms, as well as behavioral and cognitive dysfunction. It is a pathoetiologically heterogeneous disorder involving complex interrelated mechanisms that include oxidative stress and neuroinflammation. Neurovascular endothelial dysfunction and blood-brain barrier (BBB) hyperpermeability are established mechanisms in neurological disorders with comorbid psychiatric symptoms such as epilepsy, traumatic brain injury, and Alzheimer's disease. Schizophrenia is frequently comorbid with medical conditions associated with peripheral vascular endothelial dysfunction, such as metabolic syndrome, cardiovascular disease, and diabetes mellitus. However, the existence and etiological relevance of neurovascular endothelial dysfunction and BBB hyperpermeability in schizophrenia are still not well recognized. Here, we review the growing clinical and experimental evidence, indicating that neurovascular endotheliopathy and BBB hyperpermeability occur in schizophrenia patients. We present a theoretical integration of human and animal data linking oxidative stress and neuroinflammation to neurovascular endotheliopathy and BBB breakdown in schizophrenia. These abnormalities may contribute to the cognitive and behavioral symptoms of schizophrenia

Indexed as

blood–brain barrierendothelial cellendothelial nitric oxide synthaseneuroinflammationneurovascular unitnitric oxide synthaseoxidative stressschizophrenia

Identifiers

PMID28588507
PMCPMC5440518
OpenAlexW2618788509

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.