Evidence map›Paper›PMID 22015915›Full record

ReviewExperimental neurology2013

Mammalian target of rapamycin (mTOR) activation in focal cortical dysplasia and related focal cortical malformations.

Michael Wong

Open access · greenAbstract readReview
In one paragraph

Review in Experimental neurology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 11% 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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 56 citations in OpenAlex.

  1. Pooled it
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  15. Somatic overgrowth disorders of the PI3K/AKT/mTOR pathway & therapeutic strategies.American journal of medical genetics. Part C, Seminars in medical genetics · 2016
    Review
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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.

Michael WongDepartment of Neurology and the Hope Center for Neurological Disorders, Washington University School of Medicine, St. Louis, MO 63110, USA. wong_m@wustl.edu
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
NINDS NIH HHS R01 NS056872
6 · The paper itself

Abstract

Focal cortical dysplasia (FCD) and other localized malformations of cortical development represent common causes of intractable pediatric epilepsy. Insights into the cellular and molecular pathogenesis of focal cortical malformations may reveal information about associated mechanisms of epileptogenesis and suggest new therapies for seizures caused by these developmental lesions. In animal models and human studies of FCD and the related disease of Tuberous Sclerosis Complex (TSC), the mammalian target of rapamycin (mTOR) pathway has been implicated in mediating cellular and molecular changes leading to the formation of the cortical malformations and the expression of epilepsy. The use of mTOR inhibitors may represent a rational therapeutic strategy for treating or even preventing epilepsy due to FCD and TSC.

Indexed as

AnimalsHumansMalformations of Cortical DevelopmentSignal TransductionTOR Serine-Threonine KinasesTuberous SclerosisMTOR protein, humanTOR Serine-Threonine Kinases

Identifiers

PMID22015915
PMCPMC3265661
OpenAlexW2093650339

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.