Evidence map›Paper›PMID 36599709›Full record

ReviewBrain pathology (Zurich, Switzerland)2023

The neurovasculature as a target in temporal lobe epilepsy.

Yvonne Reiss, Sebastian Bauer, Bastian David, Kavi Devraj, Elif Fidan, Elke Hattingen, Stefan Liebner, Nico Melzer, Sven G Meuth, Felix Rosenow and 3 more

Open access · goldAbstract readReview
In one paragraph

Review in Brain pathology (Zurich, Switzerland), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
5.3field-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

33 citing papers in PubMed, 43 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

13 authors at 3 institutions in 1 country.

Yvonne ReissInstitute of Neurology (Edinger Institute), University Hospital, Goethe University, Frankfurt, Germany.ORCID 0000-0002-6753-7502
Sebastian BauerCenter for Personalized Translational Epilepsy Research (CePTER), University Hospital, Goethe University, Frankfurt, Germany.
Bastian DavidDepartment of Epileptology, University Hospital Bonn, Bonn, Germany.
Kavi DevrajInstitute of Neurology (Edinger Institute), University Hospital, Goethe University, Frankfurt, Germany.ORCID 0000-0002-5005-3413
Elif FidanInstitute of Neurology (Edinger Institute), University Hospital, Goethe University, Frankfurt, Germany.
Elke HattingenCenter for Personalized Translational Epilepsy Research (CePTER), University Hospital, Goethe University, Frankfurt, Germany.
Stefan LiebnerInstitute of Neurology (Edinger Institute), University Hospital, Goethe University, Frankfurt, Germany.
Nico MelzerDepartment of Neurology, Heinrich-Heine University of Düsseldorf, Düsseldorf, Germany.
Sven G MeuthDepartment of Neurology, Heinrich-Heine University of Düsseldorf, Düsseldorf, Germany.
Felix RosenowCenter for Personalized Translational Epilepsy Research (CePTER), University Hospital, Goethe University, Frankfurt, Germany.
Theodor RüberCenter for Personalized Translational Epilepsy Research (CePTER), University Hospital, Goethe University, Frankfurt, Germany.
Laurent M WillemsCenter for Personalized Translational Epilepsy Research (CePTER), University Hospital, Goethe University, Frankfurt, Germany.
Karl H PlateInstitute of Neurology (Edinger Institute), University Hospital, Goethe University, Frankfurt, Germany.
Goethe University Frankfurt · DEHeinrich Heine University Düsseldorf · DEUniversity Hospital Bonn · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The blood-brain barrier (BBB) is a physiological barrier maintaining a specialized brain micromilieu that is necessary for proper neuronal function. Endothelial tight junctions and specific transcellular/efflux transport systems provide a protective barrier against toxins, pathogens, and immune cells. The barrier function is critically supported by other cell types of the neurovascular unit, including pericytes, astrocytes, microglia, and interneurons. The dysfunctionality of the BBB is a hallmark of neurological diseases, such as ischemia, brain tumors, neurodegenerative diseases, infections, and autoimmune neuroinflammatory disorders. Moreover, BBB dysfunction is critically involved in epilepsy, a brain disorder characterized by spontaneously occurring seizures because of abnormally synchronized neuronal activity. While resistance to antiseizure drugs that aim to reduce neuronal hyperexcitability remains a clinical challenge, drugs targeting the neurovasculature in epilepsy patients have not been explored. The use of novel imaging techniques permits early detection of BBB leakage in epilepsy; however, the detailed mechanistic understanding of causes and consequences of BBB compromise remains unknown. Here, we discuss the current knowledge of BBB involvement in temporal lobe epilepsy with the emphasis on the neurovasculature as a therapeutic target.

Indexed as

EpilepsyEpilepsy, Temporal LobeAstrocytesBlood-Brain BarrierBrainHumansangiopoietin/Tie2blood-brain barriercerebral edemaepilepsy animal modelsin vitro BBB modelsneurovascular unittemporal lobe epilepsyVEGF/VEGFRWnt/β-catenin

Identifiers

PMID36599709
PMCPMC10041171
OpenAlexW4313545547

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.