Evidence map›Paper›PMID 38049961›Full record

ArticleEpilepsia2024

Cerebral vascular and blood brain-barrier abnormalities in a mouse model of epilepsy and tuberous sclerosis complex.

Dongjun Guo, Bo Zhang, Lirong Han, Nicholas R Rensing, Michael Wong

Open access · greenAbstract read
In one paragraph

Article in Epilepsia, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
4.6field-weighted citation impact, top 4% 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

14 citing papers in PubMed, 24 citations in OpenAlex.

  1. Trial
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  5. NEAT1 Promotes Epileptogenesis in Tuberous Sclerosis Complex.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Dongjun GuoDepartment of Neurology and Hope Center for Neurological Disorders, Washington University School of Medicine, St. Louis, Missouri, USA.
Bo ZhangDepartment of Neurology and Hope Center for Neurological Disorders, Washington University School of Medicine, St. Louis, Missouri, USA.
Lirong HanDepartment of Neurology and Hope Center for Neurological Disorders, Washington University School of Medicine, St. Louis, Missouri, USA.
Nicholas R RensingDepartment of Neurology and Hope Center for Neurological Disorders, Washington University School of Medicine, St. Louis, Missouri, USA.
Michael WongDepartment of Neurology and Hope Center for Neurological Disorders, Washington University School of Medicine, St. Louis, Missouri, USA.ORCID https://orcid.org/0000-0002-3796-743X
Hope Center for Neurological Disorders · US

Funding

WUIDDRC Supplement-Supporting the health and well-being of children with intellectual and developmental disability during COVID-19 pandemicP50HD103525 · NICHD · WASHINGTON UNIVERSITY · PI JOSEPH D DOUGHERTY, Natasha Marrus · 2020 to 2026
$15.5M
MECHANISMS OF BRAIN DYSFUNCTION IN TUBEROUS SCLEROSISR01NS056872 · NINDS · WASHINGTON UNIVERSITY · PI WONG, MICHAEL · 2006 to 2019
$4.0M
WHOLE SLIDE IMAGING SYSTEM FOR TRANSLATIONAL NEUROSCIENCES10RR027552 · NCRR · WASHINGTON UNIVERSITY · PI LEE, JIN-MOO · 2010 to 2010
$275k
NCRR NIH HHS S10 RR027552NICHD NIH HHS P50 HD103525NINDS NIH HHS R01 NS056872NINDS NIH HHS S10 RR027552
6 · The paper itself

Abstract

objectiveTuberous sclerosis complex (TSC) is a genetic disorder, characterized by tumor formation in the brain and other organs, and severe neurological symptoms, such as epilepsy. Abnormal vascular endothelial growth factor (VEGF) expression may promote angiogenesis in kidney and lung tumors in TSC and has been identified in brain specimens from TSC patients, but the role of VEGF and vascular abnormalities in neurological manifestations of TSC is poorly defined. In this study, we investigated abnormalities in brain VEGF expression, cerebral blood vessel anatomy, and blood-brain barrier (BBB) structure and function in a mouse model of TSC.

methodsTsc1

resultsVEGF expression was elevated in cortex of Tsc1 SIGNIFICANCE: Increased brain VEGF expression is dependent on mTOR pathway activation and promotes cerebral vascular abnormalities and increased BBB permeability in a mouse model of TSC. BBB modulation may affect epileptogenesis and represent a rational treatment for epilepsy in TSC.

Indexed as

EpilepsyTuberous SclerosisAnimalsBlood-Brain BarrierHumansMiceReceptors, Vascular Endothelial Growth FactorSeizuresSirolimusTOR Serine-Threonine KinasesTuberous Sclerosis Complex 1 ProteinTumor Suppressor ProteinsVascular Endothelial Growth Factor AReceptors, Vascular Endothelial Growth FactorSirolimusTOR Serine-Threonine KinasesTuberous Sclerosis Complex 1 ProteinTumor Suppressor ProteinsVascular Endothelial Growth Factor AmTORrapamycinseizurevascular endothelial growth factor

Identifiers

PMID38049961
PMCPMC10922951
OpenAlexW4389343815

What OpenQuestion holds

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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.