Evidence map›Paper›PMID 30625365›Full record

ArticleNeurobiology of disease2019

Human and rodent temporal lobe epilepsy is characterized by changes in O-GlcNAc homeostasis that can be reversed to dampen epileptiform activity.

Richard G Sánchez, R Ryley Parrish, Megan Rich, William M Webb, Roxanne M Lockhart, Kazuhito Nakao, Lara Ianov, Susan C Buckingham, Devin R Broadwater, Alistair Jenkins and 5 more

Open access · greenAbstract read
In one paragraph

Article in Neurobiology of disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

20 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
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  4. Review
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  6. Review
  7. Dynamic glycosylation remodeling in neurological disorders.Frontiers in molecular neuroscience · 2025
    Review
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  12. Article
  13. Brain on food: The neuroepigenetics of nutrition.Neurochemistry international · 2021
    Review
  14. Role ofPhysiological reviews · 2021
    Review
  15. Article
  16. Article
  17. Neuroproteomics in Epilepsy: What Do We Know so Far?Frontiers in molecular neuroscience · 2020
    Review
  18. Article
  19. Article
  20. Article
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

15 authors at 5 institutions in 2 countries.

Richard G SánchezDepartment of Neurobiology, University of Alabama, Birmingham, AL, United States.
R Ryley ParrishInstitute of Neuroscience, Newcastle University, Newcastle upon Tyne, UK.
Megan RichDepartment of Neurobiology, University of Alabama, Birmingham, AL, United States.
William M WebbDepartment of Neurobiology, University of Alabama, Birmingham, AL, United States.
Roxanne M LockhartDepartment of Neurobiology, University of Alabama, Birmingham, AL, United States.
Kazuhito NakaoDepartment of Neurobiology, University of Alabama, Birmingham, AL, United States.
Lara IanovCivitan International Research Center, University of Alabama, Birmingham, AL, United States.
Susan C BuckinghamDepartment of Neurobiology, University of Alabama, Birmingham, AL, United States.
Devin R BroadwaterSchool of Medicine, University of Alabama, Birmingham, AL, United States.
Alistair JenkinsDepartment of Neurosurgery, Royal Victoria Infirmary, Newcastle upon Tyne NE1 4LP, UK.
Nihal C de LanerolleDepartment of Laboratory Medicine and of Neurosurgery, Yale School of Medicine, New Haven, CT, United States.
Mark CunninghamInstitute of Neuroscience, Newcastle University, Newcastle upon Tyne, UK.
Tore EidDepartment of Laboratory Medicine and of Neurosurgery, Yale School of Medicine, New Haven, CT, United States.
Kristen RileyDepartment of Neurosurgery, University of Alabama, Birmingham, AL, United States.
Farah D LubinDepartment of Neurobiology, University of Alabama, Birmingham, AL, United States. Electronic address: flubin@uab.edu.
University of Alabama at Birmingham · USNewcastle University · GBYale University · USRoyal Victoria Infirmary · GBUniversity of Alabama · US

Funding

Yale Clinical and Translational Science Award (U Component)UL1TR001863 · NCATS · YALE UNIVERSITY · PI John H. Krystal, LUCILA OHNO-MACHADO · 2016 to 2026
$102.9M
UAB Research Training Program in Neurobiology of Cognition and Cognitive DisordersT32NS061788 · NINDS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Farah Dominique Lubin · 2008 to 2026
$4.5M
UAB Neuroscience Roadmap Scholars ProgramR25NS089463 · NINDS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI LUBIN, FARAH DOMINIQUE · 2014 to 2024
$2.7M
Chromatin Remodeling Mechanism of Gene Transcription in MemoryR56MH097909 · NIMH · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI LUBIN, FARAH DOMINIQUE · 2018 to 2018
$502k
Epigenetic Mechanisms in Epilepsy-Related Memory FormationR21NS090250 · NINDS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI LUBIN, FARAH DOMINIQUE · 2015 to 2016
$404k
NCATS NIH HHS UL1 TR001863NIMH NIH HHS R56 MH097909NINDS NIH HHS R21 NS090250NINDS NIH HHS R25 NS089463NINDS NIH HHS T32 NS061788
6 · The paper itself

Abstract

Temporal Lobe Epilepsy (TLE) is frequently associated with changes in protein composition and post-translational modifications (PTM) that exacerbate the disorder. O-linked-β-N-acetyl glucosamine (O-GlcNAc) is a PTM occurring at serine/threonine residues that is derived from and closely associated with metabolic substrates. The enzymes O-GlcNActransferase (OGT) and O-GlcNAcase (OGA) mediate the addition and removal, respectively, of the O-GlcNAc modification. The goal of this study was to characterize OGT/OGA and protein O-GlcNAcylation in the epileptic hippocampus and to determine and whether direct manipulation of these proteins and PTM's alter epileptiform activity. We observed reduced global and protein specific O-GlcNAcylation and OGT expression in the kainate rat model of TLE and in human TLE hippocampal tissue. Inhibiting OGA with Thiamet-G elevated protein O-GlcNAcylation, and decreased both seizure duration and epileptic spike events, suggesting that OGA may be a therapeutic target for seizure control. These findings suggest that loss of O-GlcNAc homeostasis in the kainate model and in human TLE can be reversed via targeting of O-GlcNAc related pathways.

Indexed as

AnimalsEpilepsy, Temporal LobeGlucosamineHippocampusHistone AcetyltransferasesHomeostasisHumansMaleN-AcetylglucosaminyltransferasesProtein Processing, Post-TranslationalRatsRats, Sprague-DawleyGlucosamineHistone AcetyltransferasesN-AcetylglucosaminyltransferasesUDP-N-acetylglucosamine-peptide beta-N-acetylglucosaminyltransferaseElectroencephalogramElectrophysiologyHippocampusMagnetic resonance imagingMass spectrometryO-GlcNAcylationPost-translational modificationThiamet-G

Identifiers

PMID30625365
PMCPMC6379093
OpenAlexW2951887812

What OpenQuestion holds

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Registered trials

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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.