Evidence map›Paper›PMID 24149933›Full record

ArticleJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism2014

Blood glutamate scavenging as a novel neuroprotective treatment for paraoxon intoxication.

Angela Ruban, Boaz Mohar, Ghil Jona, Vivian I Teichberg

Open access · bronzeAbstract read
In one paragraph

Article in Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
5.1field-weighted citation impact, top 6% 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

10 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Article
  3. Characterization of the L-glutamate clearance pathways across the blood-brain barrier and the effect of astrocytes in an in vitro blood-brain barrier model.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2017
    Article
  4. Glutamate, T cells and multiple sclerosis.Journal of neural transmission (Vienna, Austria : 1996) · 2017
    Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Brain to blood glutamate scavenging as a novel therapeutic modality: a review.Journal of neural transmission (Vienna, Austria : 1996) · 2014
    Review
  10. Is there a role for glutamate-mediated excitotoxicity in inflammation-induced depression?Journal of neural transmission (Vienna, Austria : 1996) · 2014
    Review
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

4 authors at 1 institution in 1 country.

Angela RubanDepartment of Neurobiology, Weizmann Institute of Science, Rehovot, Israel.
Boaz MoharDepartment of Neurobiology, Weizmann Institute of Science, Rehovot, Israel.
Ghil JonaDepartment of Biological services, Weizmann Institute of Science, Rehovot, Israel.
Vivian I TeichbergDepartment of Neurobiology, Weizmann Institute of Science, Rehovot, Israel.
Weizmann Institute of Science · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Organophosphate-induced brain damage is an irreversible neuronal injury, likely because there is no pharmacological treatment to prevent or block secondary damage processes. The presence of free glutamate (Glu) in the brain has a substantial role in the propagation and maintenance of organophosphate-induced seizures, thus contributing to the secondary brain damage. This report describes for the first time the ability of blood glutamate scavengers (BGS) oxaloacetic acid in combination with glutamate oxaloacetate transaminase to reduce the neuronal damage in an animal model of paraoxon (PO) intoxication. Our method causes a rapid decrease of blood Glu levels and creates a gradient that leads to the efflux of the excess brain Glu into the blood, thus reducing neurotoxicity. We demonstrated that BGS treatment significantly prevented the peripheral benzodiazepine receptor (PBR) density elevation, after PO exposure. Furthermore, we showed that BGS was able to rescue neurons in the piriform cortex of the treated rats. In conclusion, these results suggest that treatment with BGS has a neuroprotective effect in the PO intoxication. This is the first time that this approach is used in PO intoxication and it may be of high clinical significance for the future treatment of the secondary neurologic damage post organophosphates exposure.

Indexed as

Brain InjuriesAnimalsAspartate AminotransferasesCarrier ProteinsCerebral CortexCholinesterase InhibitorsDisease Models, AnimalHep G2 CellsHumansMaleNeuronsOxaloacetic AcidParaoxonRatsRats, Sprague-DawleyReceptors, GABA-AAspartate AminotransferasesCarrier ProteinsCholinesterase InhibitorsOxaloacetic AcidParaoxonReceptors, GABA-ATspo protein, rat

Identifiers

PMID24149933
PMCPMC3915200
OpenAlexW1992357222

What OpenQuestion holds

Textmetadata
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.