Evidence map›Paper›PMID 29044647›Full record

ReviewGlia2018

Epilepsy and astrocyte energy metabolism.

Detlev Boison, Christian Steinhäuser

Open access · bronzeAbstract readReview
In one paragraph

Review in Glia, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 147 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
147citing papers in PubMed, 2 pooled it
8.9field-weighted citation impact, top 2% 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

147 citing papers in PubMed, 2 syntheses or guidelines pooled it, 240 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Modern Analytical Techniques in Epilepsy Research.International journal of molecular sciences · 2026
    Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article

87 more citing papers are in PubMed but not listed here.

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

2 authors at 2 institutions in 2 countries.

Detlev BoisonR.S. Dow Neurobiology Laboratories, Legacy Research Institute, Portland, Oregon.
Christian SteinhäuserInstitute of Cellular Neurosciences, Medical Faculty, University of Bonn, Germany.ORCID 0000-0003-2579-8357
Legacy Health · USUniversity of Bonn · DE

Funding

Glycine augmentation therapy for the treatment of epilepsyR01NS084920 · NINDS · LEGACY EMANUEL HOSPITAL AND HEALTH CENTER · PI SHEN, HAIYING · 2014 to 2018
$1.8M
Adenosine receptor mediated therapies for SUDEPR01NS103740 · NINDS · RBHS-ROBERT WOOD JOHNSON MEDICAL SCHOOL · PI BOISON, DETLEV · 2018 to 2022
$1.7M
Astrocyte dysfunction in epileptogenesis: the role of adenosineR01NS061844 · NINDS · LEGACY EMANUEL HOSPITAL AND HEALTH CENTER · PI BOISON, DETLEV · 2009 to 2013
$1.5M
Adenosine kinase antisense gene therapy for temporal lobe epilepsy.R21NS088024 · NINDS · LEGACY EMANUEL HOSPITAL AND HEALTH CENTER · PI BOISON, DETLEV · 2015 to 2016
$825k
NINDS NIH HHS R01 NS061844NINDS NIH HHS R01 NS084920NINDS NIH HHS R01 NS103740NINDS NIH HHS R21 NS088024
6 · The paper itself

Abstract

Epilepsy is a complex neurological syndrome characterized by neuronal hyperexcitability and sudden, synchronized electrical discharges that can manifest as seizures. It is now increasingly recognized that impaired astrocyte function and energy homeostasis play key roles in the pathogenesis of epilepsy. Excessive neuronal discharges can only happen, if adequate energy sources are made available to neurons. Conversely, energy depletion during seizures is an endogenous mechanism of seizure termination. Astrocytes control neuronal energy homeostasis through neurometabolic coupling. In this review, we will discuss how astrocyte dysfunction in epilepsy leads to distortion of key metabolic and biochemical mechanisms. Dysfunctional glutamate metabolism in astrocytes can directly contribute to neuronal hyperexcitability. Closure of astrocyte intercellular gap junction coupling as observed early during epileptogenesis limits activity-dependent trafficking of energy metabolites, but also impairs clearance of the extracellular space from accumulation of K

Indexed as

Energy MetabolismAnimalsAstrocytesEpilepsyHumansNeuronsadenosinegap junction couplingketogenic dietlactateneuron-glia interaction

Identifiers

PMID29044647
PMCPMC5903956
OpenAlexW2765406496

What OpenQuestion holds

Textmetadata
LicenceTDM
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.