Evidence map›Paper›PMID 24525730›Full record

ArticleCell death & disease2014

Early and sustained altered expression of aging-related genes in young 3xTg-AD mice.

V Gatta, M D'Aurora, A Granzotto, L Stuppia, S L Sensi

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death & disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 12% 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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.

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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

5 authors at 2 institutions in 2 countries.

V Gatta1] Functional Genetics Unit, Center of Excellence on Aging (CeSI), Chieti, Italy [2] Department of Psychological Sciences, 'G. d'Annunzio' University, Chieti, Italy.
M D'Aurora1] Functional Genetics Unit, Center of Excellence on Aging (CeSI), Chieti, Italy [2] Department of Neuroscience and Imaging, 'G. d'Annunzio' University, Chieti, Italy.
A GranzottoMolecular Neurology Unit, Center of Excellence on Aging (CeSI), Chieti, Italy.ORCID 0000000191814373
L Stuppia1] Functional Genetics Unit, Center of Excellence on Aging (CeSI), Chieti, Italy [2] Department of Psychological Sciences, 'G. d'Annunzio' University, Chieti, Italy.
S L Sensi1] Department of Neuroscience and Imaging, 'G. d'Annunzio' University, Chieti, Italy [2] Molecular Neurology Unit, Center of Excellence on Aging (CeSI), Chieti, Italy [3] Departments of Neurology and Pharmacology, University of California-Irvine, Irvine, CA, USA [4] Institute for Memory Impairments and Neurological Disorders, University of California-Irvine, Irvine, CA, USA.
University of Chieti-Pescara · ITUniversity of California, Irvine · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is a multifactorial neurological condition associated with a genetic profile that is still not completely understood. In this study, using a whole gene microarray approach, we investigated age-dependent gene expression profile changes occurring in the hippocampus of young and old transgenic AD (3xTg-AD) and wild-type (WT) mice. The aim of the study was to assess similarities between aging- and AD-related modifications of gene expression and investigate possible interactions between the two processes. Global gene expression profiles of hippocampal tissue obtained from 3xTg-AD and WT mice at 3 and 12 months of age (m.o.a.) were analyzed by hierarchical clustering. Interaction among transcripts was then studied with the Ingenuity Pathway Analysis (IPA) software, a tool that discloses functional networks and/or pathways associated with sets of specific genes of interest. Cluster analysis revealed the selective presence of hundreds of upregulated and downregulated transcripts. Functional analysis showed transcript involvement mainly in neuronal death and autophagy, mitochondrial functioning, intracellular calcium homeostasis, inflammatory response, dendritic spine formation, modulation of synaptic functioning, and cognitive decline. Thus, overexpression of AD-related genes (such as mutant APP, PS1, and hyperphosphorylated tau, the three genes that characterize our model) appears to favor modifications of additional genes that are involved in AD development and progression. The study also showed overlapping changes in 3xTg-AD at 3 m.o.a. and WT mice at 12 m.o.a., thereby suggesting altered expression of aging-related genes that occurs earlier in 3xTg-AD mice.

Indexed as

Age FactorsAgingAlzheimer DiseaseAmyloid beta-Protein PrecursorAnimalsCluster AnalysisDisease Models, AnimalFemaleGene Expression ProfilingGene Expression RegulationGene Regulatory NetworksGenetic Predisposition to DiseaseHippocampusHumansMiceMice, 129 StrainAmyloid beta-Protein PrecursorPresenilin-1tau Proteins

Identifiers

PMID24525730
PMCPMC3944230
OpenAlexW2071462548

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.