Evidence map›Paper›PMID 25663420›Full record

ArticleAge (Dordrecht, Netherlands)2015

Amyloid and tau pathology of familial Alzheimer's disease APP/PS1 mouse model in a senescence phenotype background (SAMP8).

D Porquet, P Andrés-Benito, C Griñán-Ferré, A Camins, I Ferrer, A M Canudas, J Del Valle, Mercè Pallàs

Open access · greenAbstract read
In one paragraph

Article in Age (Dordrecht, Netherlands), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

27 citing papers in PubMed, 60 citations in OpenAlex.

  1. Review
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  6. Review
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  11. Neuroprotective Effects ofJournal of immunology research · 2021
    Article
  12. Article
  13. Article
  14. Review
  15. MicroalgaeFrontiers in cell and developmental biology · 2020
    Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Rodent models for Alzheimer disease.Nature reviews. Neuroscience · 2018
    Review
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

8 authors at 2 institutions in 1 country.

D PorquetSecció de Farmacologia, Departament Farmacologia i Química Terapèutica, Facultat de Farmàcia, Institut de Biomedicina (IBUB), Universitat de Barcelona (UB), Av. Diagonal 643, 08028, Barcelona, Spain.
P Andrés-Benito
C Griñán-Ferré
A Camins
I Ferrer
A M Canudas
J Del Valle
Mercè Pallàs
Biomedical Research Networking Center on Neurodegenerative Diseases · ESUniversitat de Barcelona · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The amyloid precursor protein/presenilin 1 (APP/PS1) mouse model of Alzheimer's disease (AD) has provided robust neuropathological hallmarks of familial AD-like pattern at early ages, whereas senescence-accelerated mouse prone 8 (SAMP8) has a remarkable early senescence phenotype with pathological similarities to AD. The aim of this study was the investigation and characterization of cognitive and neuropathological AD markers in a novel mouse model that combines the characteristics of the APP/PS1 transgenic mouse model with a senescence-accelerated background of SAMP8 mice. Initially, significant differences were found regarding amyloid plaque formation and cognitive abnormalities. Bearing these facts in mind, we determined a general characterization of the main AD brain molecular markers, such as alterations in amyloid pathway, neuroinflammation, and hyperphosphorylation of tau in these mice along their lifetimes. Results from this analysis revealed that APP/PS1 in SAMP8 background mice showed alterations in the pathways studied in comparison with SAMP8 and APP/PS1, demonstrating that a senescence-accelerated background exacerbated the amyloid pathology and maintained the cognitive dysfunction present in APP/PS1 mice. Changes in tau pathology, including the activity of cyclin-dependent kinase 5 (CDK5) and glycogen synthase kinase 3 β (GSK3β), differs, but not in a parallel manner, with amyloid disturbances.

Indexed as

AgingAlzheimer DiseaseAmyloid beta-Protein PrecursorAnimalsDisease Models, AnimalMiceMice, TransgenicPhenotypePresenilin-1tau ProteinsAmyloid beta-Protein PrecursorPresenilin-1presenilin 1, mousetau Proteins

Identifiers

PMID25663420
PMCPMC4320125
OpenAlexW2071167787

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.