Evidence map›Paper›PMID 36077024›Full record

ReviewInternational journal of molecular sciences2022

Glutamate Neurotoxicity and Destruction of the Blood-Brain Barrier: Key Pathways for the Development of Neuropsychiatric Consequences of TBI and Their Potential Treatment Strategies.

Benjamin F Gruenbaum, Alexander Zlotnik, Ilya Fleidervish, Amit Frenkel, Matthew Boyko

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 2 pooled it
4.3field-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

37 citing papers in PubMed, 2 syntheses or guidelines pooled it, 49 citations in OpenAlex.

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  15. Metabolomics of cerebrospinal fluid following traumatic brain injury: Exploration of biomarkers for secondary injuries and severity.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
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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.

Benjamin F GruenbaumDepartment of Anesthesiology and Perioperative Medicine, Mayo Clinic, Jacksonville, FL 32224, USA.
Alexander ZlotnikDepartment of Anesthesiology and Critical Care, Soroka University Medical Center, Ben-Gurion of the Negev, Beer-Sheva 84105, Israel.
Ilya FleidervishDepartment of Physiology and Cell Biology, Faculty of Health Sciences and Zlotowski Center for Neuroscience, Ben-Gurion University of the Negev, Beer-Sheva 84105, Israel.
Amit FrenkelDepartment of Anesthesiology and Critical Care, Soroka University Medical Center, Ben-Gurion of the Negev, Beer-Sheva 84105, Israel.ORCID 0000-0002-4162-8406
Matthew BoykoDepartment of Anesthesiology and Critical Care, Soroka University Medical Center, Ben-Gurion of the Negev, Beer-Sheva 84105, Israel.ORCID 0000-0003-3116-1643
Soroka Medical Center · ILBen-Gurion University of the Negev · ILMayo Clinic in Florida · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Traumatic brain injury (TBI) is associated with significant cognitive and psychiatric conditions. Neuropsychiatric symptoms can persist for years following brain injury, causing major disruptions in patients' lives. In this review, we examine the role of glutamate as an aftereffect of TBI that contributes to the development of neuropsychiatric conditions. We hypothesize that TBI causes long-term blood-brain barrier (BBB) dysfunction lasting many years and even decades. We propose that dysfunction in the BBB is the central factor that modulates increased glutamate after TBI and ultimately leads to neurodegenerative processes and subsequent manifestation of neuropsychiatric conditions. Here, we have identified factors that determine the upper and lower levels of glutamate concentration in the brain after TBI. Furthermore, we consider treatments of disruptions to BBB integrity, including repairing the BBB and controlling excess glutamate, as potential therapeutic modalities for the treatment of acute and chronic neuropsychiatric conditions and symptoms. By specifically focusing on the BBB, we hypothesize that restoring BBB integrity will alleviate neurotoxicity and related neurological sequelae.

Indexed as

Brain InjuriesBrain Injuries, TraumaticNeurotoxicity SyndromesBlood-Brain BarrierBrainGlutamic AcidHumansGlutamic Acidblood–brain barrier (BBB)blood glutamate scavengersglutamateneuropsychiatric conditionstraumatic brain injury (TBI)

Identifiers

PMID36077024
PMCPMC9456007
OpenAlexW4293103509

What Socratic 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 Socratic graph.