Evidence map›Paper›PMID 24001064›Full record

ReviewEpilepsia2013

Role of adenosine in status epilepticus: a potential new target?

Detlev Boison

Open access · bronzeAbstract readReview
In one paragraph

Review in Epilepsia, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
5.1field-weighted citation impact, top 5% 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

21 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Spinal AJournal of neuroscience research · 2022
    Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Pain and Poppies: The Good, the Bad, and the Ugly of Opioid Analgesics.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015
    Review
  16. Initiation, Propagation, and Termination of Partial (Focal) Seizures.Cold Spring Harbor perspectives in medicine · 2015
    Review
  17. Review
  18. Article
  19. Refractory status epilepticus.Annals of Indian Academy of Neurology · 2014
    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

1 author at 1 institution in 1 country.

Detlev BoisonRobert Stone Dow Neurobiology Laboratories, Legacy Research Institute, 1225 NE 2nd Ave, Portland, OR 97232, U.S.A. dboison@downeurobiology.org
Legacy Health · US

Funding

The Role of Adenosine in Ketogenic Diet TherapyR01NS065957 · NINDS · TRINITY COLLEGE · PI BOISON, DETLEV, GEIGER, JONATHAN DAVID · 2010 to 2021
$3.9M
Astrocyte dysfunction in epileptogenesis: the role of adenosineR01NS061844 · NINDS · LEGACY EMANUEL HOSPITAL AND HEALTH CENTER · PI BOISON, DETLEV · 2009 to 2013
$1.5M
Adenosine-releasing brain implants for epilepsy therapyR01NS058780 · NINDS · LEGACY EMANUEL HOSPITAL AND HEALTH CENTER · PI BOISON, DETLEV · 2008 to 2011
$1.2M
NINDS NIH HHS NS061844NINDS NIH HHS NS065957NINDS NIH HHS R01 NS058780NINDS NIH HHS R01 NS061844NINDS NIH HHS R01 NS065957
6 · The paper itself

Abstract

The homeostatic bioenergetic network regulator adenosine is an endogenous anticonvulsant of the brain that plays critical roles in seizure termination and postictal refractoriness. Adenosine homeostasis in the adult brain is largely under the control of metabolic clearance through adenosine kinase (ADK), expressed predominantly in astrocytes. The role of adenosine in status epilepticus (SE) appears to be a double-edged sword. We demonstrated that the severity of an SE clearly depends on the expression levels of ADK. A genetic knockdown of ADK prevented SE in a mouse model, whereas transgenic overexpression of the enzyme aggravated the SE. Therefore, ADK inhibition or adenosine augmentation might be a therapeutic strategy to terminate or attenuate an SE. On the other hand, SE triggers a surge of endogenous adenosine, which may initiate secondary events leading to epileptogenesis. Two new findings point into this direction: (1) Elevated adenosine triggers changes in the epigenome; and (2) SE triggers transient changes in ADK expression, which have been linked to neurogenesis. Although the ADK/adenosine system is an attractive target for the attenuation of an SE, the same system may also trigger downstream events related to epileptogenesis.

Indexed as

AdenosineAdenosine KinaseAnimalsAstrocytesHumansStatus EpilepticusAdenosineAdenosine KinaseAdenosineAdenosine augmentation therapyAdenosine kinaseEpigeneticsNeurogenesis

Identifiers

PMID24001064
PMCPMC3767194
OpenAlexW2162984354

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.