Evidence map›Paper›PMID 21354266›Full record

ReviewNeuroscience letters2011

Therapeutic role of mammalian target of rapamycin (mTOR) inhibition in preventing epileptogenesis.

Sharon S McDaniel, Michael Wong

Open access · greenAbstract readReview
In one paragraph

Review in Neuroscience letters, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
5.7field-weighted citation impact, top 3% 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

44 citing papers in PubMed, 75 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Anticonvulsant Activity ofMolecules (Basel, Switzerland) · 2022
    Article
  6. Review
  7. Article
  8. Insights into Potential Targets for Therapeutic Intervention in Epilepsy.International journal of molecular sciences · 2020
    Review
  9. Article
  10. Review
  11. Effects of antiepileptic drugs in a new TSC/mTOR-dependent epilepsy mouse model.Annals of clinical and translational neurology · 2019
    Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Review
  17. Article
  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

2 authors at 1 institution in 1 country.

Sharon S McDanielDepartment of Neurology and the Hope Center for Neurological Disorders, Washington University School of Medicine, St. Louis, MO 63110, USA.
Michael Wong
Hope Center for Neurological Disorders · US

Funding

MECHANISMS OF BRAIN DYSFUNCTION IN TUBEROUS SCLEROSISR01NS056872 · NINDS · WASHINGTON UNIVERSITY · PI WONG, MICHAEL · 2006 to 2019
$4.0M
Rapid seizure-induced changes in dendritic spinesK02NS045583 · NINDS · WASHINGTON UNIVERSITY · PI WONG, MICHAEL · 2003 to 2007
$714k
NINDS NIH HHS K02 NS045583NINDS NIH HHS R01 NS056872
6 · The paper itself

Abstract

Traditionally, medical therapy for epilepsy has aimed to suppress seizure activity, but has been unable to alter the progression of the underlying disease. Recent advances in our understanding of mechanisms of epileptogenesis open the door for the development of new therapies which prevent the pathogenic changes in the brain that predispose to spontaneous seizures. In particular, the mammalian target of rapamycin (mTOR) signaling pathway has recently garnered interest as an important regulator of cellular changes involved in epileptogenesis, and mTOR inhibitors have generated excitement as potential antiepileptogenic agents. mTOR hyperactivation occurs in tuberous sclerosis complex (TSC), a common genetic cause of epilepsy, as a result of genetic mutations in upstream regulatory molecules. mTOR inhibition prevents epilepsy and brain pathology in animal models of TSC. mTOR dysregulation has also been demonstrated in a variety of other genetic and acquired epilepsies, including brain tumors, focal cortical dysplasias, and animal models of brain injury due to status epilepticus or trauma. Indeed, mTOR inhibitors appear to possess antiepileptogenic properties in animal models of acquired epilepsy as well. Thus, mTOR dysregulation may represent a final common pathway in epilepsies of various causes. Therefore, mTOR inhibition is an exciting potential antiepileptogenic strategy with broad applications for epilepsy and could be involved in a number of treatment modalities, including the ketogenic diet. Further research is necessary to determine the clinical utility of rapamycin and other mTOR inhibitors for antiepileptogenesis, and to devise new therapeutic targets by further elucidating the signaling molecules involved in epileptogenesis.

Indexed as

AnimalsAnticonvulsantsBrainEncephalitisEpilepsyHumansTOR Serine-Threonine KinasesAnticonvulsantsMTOR protein, humanTOR Serine-Threonine Kinases

Identifiers

PMID21354266
PMCPMC3109223
OpenAlexW2061460624

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.