Evidence map›Paper›PMID 24899720›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014

Genetic reduction of mammalian target of rapamycin ameliorates Alzheimer's disease-like cognitive and pathological deficits by restoring hippocampal gene expression signature.

Antonella Caccamo, Vito De Pinto, Angela Messina, Caterina Branca, Salvatore Oddo

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 118 papers.

0numbers the graph read from it
0cells of the map it votes in
118citing papers in PubMed
10.6field-weighted citation impact, top 1% 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

118 citing papers in PubMed, 187 citations in OpenAlex.

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  6. Heavy metal-induced disruption of the autophagy-lysosomal pathway: implications for aging and neurodegenerative disorders.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2025
    Review
  7. Article
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  9. Disrupted mitochondrial response to nutrients is a presymptomatic event in the cortex of the APPAlzheimer's & dementia : the journal of the Alzheimer's Association · 2024
    Article
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  13. Dysregulation of mTOR by tau in Alzheimer's disease.Cytoskeleton (Hoboken, N.J.) · 2024
    Review
  14. Article
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58 more citing papers are in PubMed but not listed here.

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

5 authors at 2 institutions in 2 countries.

Antonella CaccamoBanner Sun Health Research Institute, Sun City, Arizona 85351, Department of Biological, Geological, and Environmental Sciences, University of Catania, 95125 Catania, Italy.
Vito De PintoDepartment of Biological, Geological, and Environmental Sciences, University of Catania, 95125 Catania, Italy.
Angela MessinaDepartment of Biological, Geological, and Environmental Sciences, University of Catania, 95125 Catania, Italy.
Caterina BrancaBanner Sun Health Research Institute, Sun City, Arizona 85351, Department of Molecular and Translational Medicine, University of Brescia, 25123 Brescia, Italy, and.
Salvatore OddoBanner Sun Health Research Institute, Sun City, Arizona 85351, Department of Basic Medical Sciences, University of Arizona College of Medicine-Phoenix, Phoenix, Arizona 85004 oddo@email.arizona.edu.
Banner Sun Health Research Institute · USUniversity of Catania · IT

Funding

Molecular interplay between Abeta, tau and mTOR: Mechanisms of neurodegenerationR01AG037637 · NIA · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI ODDO, SALVATORE · 2011 to 2015
$1.6M
NIA NIH HHS R01 AG037637
6 · The paper itself

Abstract

Elevated mammalian target of rapamycin (mTOR) signaling has been found in Alzheimer's disease (AD) patients and is linked to diabetes and aging, two known risk factors for AD. However, whether hyperactive mTOR plays a role in the cognitive deficits associated with AD remains elusive. Here, we genetically reduced mTOR signaling in the brains of Tg2576 mice, a widely used animal model of AD. We found that suppression of mTOR signaling reduced amyloid-β deposits and rescued memory deficits. Mechanistically, the reduction in mTOR signaling led to an increase in autophagy induction and restored the hippocampal gene expression signature of the Tg2576 mice to wild-type levels. Our results implicate hyperactive mTOR signaling as a previous unidentified signaling pathway underlying gene-expression dysregulation and cognitive deficits in AD. Furthermore, hyperactive mTOR signaling may represent a molecular pathway by which aging contributes to the development of AD.

Indexed as

Cognition DisordersAlzheimer DiseaseAmyloid beta-Protein PrecursorAnimalsCalcium-Calmodulin-Dependent Protein Kinase Type 2Disease Models, AnimalGene ExpressionGene Expression ProfilingGene Expression RegulationHippocampusHumansImmunosuppressive AgentsMaze LearningMiceMice, Inbred C57BLMice, TransgenicAmyloid beta-Protein PrecursorCalcium-Calmodulin-Dependent Protein Kinase Type 2Immunosuppressive AgentsTOR Serine-Threonine Kinasesamyloid-βautophagyAβplaquestanglestau

Identifiers

PMID24899720
PMCPMC4044255
OpenAlexW2071951303

What OpenQuestion holds

Textmetadata
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.