Evidence map›Paper›PMID 22848848›Full record

ReviewNeural plasticity2012

Synaptic plasticity and learning in animal models of tuberous sclerosis complex.

Timo Kirschstein

Open access · goldAbstract readReview
In one paragraph

Review in Neural plasticity, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

10 citing papers in PubMed, 14 citations in OpenAlex.

  1. 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.

Timo KirschsteinOscar Langendorff Institute of Physiology, University of Rostock, Gertrudenstrasse 9, 18057 Rostock, Germany. timo.kirschstein@uni-rostock.de
University of Rostock · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tuberous sclerosis complex (TSC) is caused by a mutation of either the Tsc1 or Tsc2 gene. As these genes work in concert to negatively regulate the mammalian target of rapamycin (mTOR) kinase which is involved in protein translation, mutations of these genes lead to a disinhibited mTOR activity. Both the clinical appearance of this condition including tumors, cognitive decline, and epileptic seizures and the molecular understanding of the mTOR signaling pathway, not only involved in cell growth, but also in neuronal functioning, have inspired numerous studies on learning behavior as well as on synaptic plasticity which is the key molecular mechanism of information storage in the brain. A couple of interesting animal models have been established, and the data obtained in these animals will be discussed. A special focus will be laid on differences among these models, which may be in part due to different background strains, but also may indicate pathophysiological variation in different mutations.

Indexed as

AnimalsDisease Models, AnimalHumansLearningMiceNeuronal PlasticityRatsSynapsesTOR Serine-Threonine KinasesTuberous SclerosisTOR Serine-Threonine Kinases

Identifiers

PMID22848848
PMCPMC3403083
OpenAlexW2045353657

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.