Evidence map›Paper›PMID 39192595›Full record

ArticleAging cell2024

Premature cognitive decline in a mouse model of tuberous sclerosis.

J Krummeich, L Nardi, C Caliendo, D Aschauer, V Engelhardt, A Arlt, J Maier, F Bicker, M D Kwiatkowski, K Rolski and 6 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Aging cell, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. 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

16 authors.

J KrummeichInstitute of Human Genetics, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.ORCID 0009-0004-7700-7320
L NardiInstitute of Anatomy, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.
C CaliendoInstitute of Human Genetics, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.
D AschauerInstitute of Physiology, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.
V EngelhardtInstitute of Human Genetics, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.
A ArltInstitute of Human Genetics, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.
J MaierInstitute of Anatomy, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.
F BickerInstitute of Anatomy, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.
M D KwiatkowskiDepartment of Biochemistry, University of Innsbruck, Innsbruck, Austria.
K RolskiDepartment of Biochemistry, University of Innsbruck, Innsbruck, Austria.
K VinczeDepartment of Biochemistry, University of Innsbruck, Innsbruck, Austria.
R SchneiderDepartment of Biochemistry, University of Innsbruck, Innsbruck, Austria.
S RumpelInstitute of Physiology, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.
S GerberInstitute of Human Genetics, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.
M J SchmeisserInstitute of Anatomy, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.
S SchweigerInstitute of Human Genetics, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.ORCID 0000-0002-7816-8984

Funding

Deutsche Forschungsgemeinschaft #431393205Deutsche Forschungsgemeinschaft CRC 1080Deutsche Forschungsgemeinschaft DIP "Neurobiology of Forgetting"Deutsche Forschungsgemeinschaft SPP 2041
6 · The paper itself

Abstract

Little is known about the influence of (impaired) neurodevelopment on cognitive aging. We here used a mouse model for tuberous sclerosis (TS) carrying a heterozygous deletion of the Tsc2 gene. Loss of Tsc2 function leads to mTOR hyperactivity in mice and patients. In a longitudinal behavioral analysis, we found premature decline of hippocampus-based cognitive functions together with a significant reduction of immediate early gene (IEG) expression. While we did not detect any morphological changes of hippocampal projections and synaptic contacts, molecular markers of neurodegeneration were increased and the mTOR signaling cascade was downregulated in hippocampal synaptosomes. Injection of IGF2, a molecule that induces mTOR signaling, could fully rescue cognitive impairment and IEG expression in aging Tsc2

Indexed as

Disease Models, AnimalTuberous SclerosisAnimalsCognitive DysfunctionHippocampusHumansInsulin-Like Growth Factor IIMaleMiceSignal TransductionTOR Serine-Threonine KinasesTuberous Sclerosis Complex 2 ProteinTumor Suppressor ProteinsIGF2 protein, mouseInsulin-Like Growth Factor IITOR Serine-Threonine KinasesTsc2 protein, mouseTuberous Sclerosis Complex 2 ProteinTumor Suppressor ProteinsagingIGF2mTORneurodegenerationpremature cognitive declinerescue

Identifiers

PMID39192595
PMCPMC11634721

What OpenQuestion holds

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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.