Evidence map›Paper›PMID 27147960›Full record

ReviewFrontiers in molecular neuroscience2016

The Biochemistry and Epigenetics of Epilepsy: Focus on Adenosine and Glycine.

Detlev Boison

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in molecular neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
5.2field-weighted citation impact, top 4% 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

35 citing papers in PubMed, 64 citations in OpenAlex.

  1. GlyT1 (SLC6A9) inhibition in neurological and psychiatric disorders.Naunyn-Schmiedeberg's archives of pharmacology · 2026
    Review
  2. Neurotransmitter Systems in Alzheimer's Disease.Current issues in molecular biology · 2026
    Review
  3. Review
  4. Article
  5. Review
  6. Review
  7. Pharmacological inhibition of ENT1 enhances the impact of specific dietary fats on energy metabolism gene expression.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  8. Brain Neuroplasticity after Treatment with Antiseizure: A Review.Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology · 2023
    Review
  9. Review
  10. Metabonomic analysis of cerebrospinal fluid in epilepsy.Annals of translational medicine · 2022
    Article
  11. Article
  12. Review
  13. Article
  14. Specialty Grand Challenge for Brain Disease Mechanisms.Frontiers in molecular neuroscience · 2021
    Article
  15. The Epigenome in Neurodevelopmental Disorders.Frontiers in neuroscience · 2021
    Review
  16. Review
  17. Article
  18. Article
  19. Review
  20. Role of Adenosine in Epilepsy and Seizures.Journal of caffeine and adenosine research · 2020
    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 Portland, OR, USA.
Legacy Health · US

Funding

Adenosine and schizophrenia: mechanisms and therapiesR01MH083973 · NIMH · LEGACY EMANUEL HOSPITAL AND HEALTH CENTER · PI BOISON, DETLEV · 2009 to 2015
$2.5M
Glycine augmentation therapy for the treatment of epilepsyR01NS084920 · NINDS · LEGACY EMANUEL HOSPITAL AND HEALTH CENTER · PI SHEN, HAIYING · 2014 to 2018
$1.8M
Adenosine kinase antisense gene therapy for temporal lobe epilepsy.R21NS088024 · NINDS · LEGACY EMANUEL HOSPITAL AND HEALTH CENTER · PI BOISON, DETLEV · 2015 to 2016
$825k
NIMH NIH HHS R01 MH083973NINDS NIH HHS R01 NS084920NINDS NIH HHS R21 NS088024
6 · The paper itself

Abstract

Epilepsy, one of the most prevalent neurological conditions, presents as a complex disorder of network homeostasis characterized by spontaneous non-provoked seizures and associated comorbidities. Currently used antiepileptic drugs have been designed to suppress neuronal hyperexcitability and thereby to suppress epileptic seizures. However, the current armamentarium of antiepileptic drugs is not effective in over 30% of patients, does not affect the comorbidities of epilepsy, and does not prevent the development and progression of epilepsy (epileptogenesis). Prevention of epilepsy and its progression remains the Holy Grail for epilepsy research and therapy development, requiring novel conceptual advances to find a solution to this urgent medical need. The methylation hypothesis of epileptogenesis suggests that changes in DNA methylation are implicated in the progression of the disease. In particular, global DNA hypermethylation appears to be associated with chronic epilepsy. Clinical as well as experimental evidence demonstrates that epilepsy and its progression can be prevented by biochemical manipulations and those that target previously unrecognized epigenetic functions contributing to epilepsy development and maintenance of the epileptic state. This mini-review will discuss, epigenetic mechanisms implicated in epileptogenesis and biochemical interactions between adenosine and glycine as a conceptual advance to understand the contribution of maladaptive changes in biochemistry as a major contributing factor to the development of epilepsy. New findings based on biochemical manipulation of the DNA methylome suggest that: (i) epigenetic mechanisms play a functional role in epileptogenesis; and (ii) therapeutic reconstruction of the epigenome is an effective antiepileptogenic therapy.

Indexed as

adenosineadenosine kinaseDNA methylationepigeneticsepilepsyepileptogenesisglycineglycine transporter 1

Identifiers

PMID27147960
PMCPMC4829603
OpenAlexW2341042891

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.