Evidence map›Paper›PMID 33927688›Full record

ReviewFrontiers in neurology2021

Astroglial Glutamine Synthetase and the Pathogenesis of Mesial Temporal Lobe Epilepsy.

Mani Ratnesh S Sandhu, Benjamin F Gruenbaum, Shaun E Gruenbaum, Roni Dhaher, Ketaki Deshpande, Melissa C Funaro, Tih-Shih W Lee, Hitten P Zaveri, Tore Eid

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in neurology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

25 citing papers in PubMed, 45 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Reactive Astrocytes in Glioma: Emerging Opportunities and Challenges.International journal of molecular sciences · 2025
    Review
  8. Review
  9. Neuroglia and brain energy metabolism.Handbook of clinical neurology · 2025
    Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. GLUL stabilizes N-Cadherin by antagonizingActa pharmaceutica Sinica. B · 2024
    Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. 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

9 authors at 3 institutions in 1 country.

Mani Ratnesh S SandhuDepartment of Laboratory Medicine, New Haven, CT, United States.
Benjamin F GruenbaumDepartment of Anesthesiology and Perioperative Medicine, Mayo Clinic, Jacksonville, FL, United States.
Shaun E GruenbaumDepartment of Anesthesiology and Perioperative Medicine, Mayo Clinic, Jacksonville, FL, United States.
Roni DhaherDepartment of Neurosurgery, New Haven, CT, United States.
Ketaki DeshpandeDepartment of Laboratory Medicine, New Haven, CT, United States.
Melissa C FunaroHarvey Cushing/John Hay Whitney Medical Library, Yale University, New Haven, CT, United States.
Tih-Shih W LeeDepartment of Psychiatry, New Haven, CT, United States.
Hitten P ZaveriDepartment of Neurology, Yale School of Medicine, New Haven, CT, United States.
Tore EidDepartment of Laboratory Medicine, New Haven, CT, United States.
University of New Haven · USMayo Clinic in Florida · USYale University · US

Funding

Network analysis for epilepsy surgeryR01NS109062 · NINDS · YALE UNIVERSITY · PI EID, TORE, ZAVERI, HITTEN P · 2019 to 2022
$1.5M
NINDS NIH HHS R01 NS109062
6 · The paper itself

Abstract

The enzyme glutamine synthetase (GS), also referred to as glutamate ammonia ligase, is abundant in astrocytes and catalyzes the conversion of ammonia and glutamate to glutamine. Deficiency or dysfunction of astrocytic GS in discrete brain regions have been associated with several types of epilepsy, including medically-intractable mesial temporal lobe epilepsy (MTLE), neocortical epilepsies, and glioblastoma-associated epilepsy. Moreover, experimental inhibition or deletion of GS in the entorhinal-hippocampal territory of laboratory animals causes an MTLE-like syndrome characterized by spontaneous, recurrent hippocampal-onset seizures, loss of hippocampal neurons, and in some cases comorbid depressive-like features. The goal of this review is to summarize and discuss the possible roles of astroglial GS in the pathogenesis of epilepsy.

Indexed as

astrocyteepilepsyepilepsy networkepileptogenesisglutamine synthetasemesial temporal lobe epilepsy

Identifiers

PMID33927688
PMCPMC8078591
OpenAlexW3153759411

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.