Evidence map›Paper›PMID 37182890›Full record

ArticleJournal of Alzheimer's disease : JAD2023

Generation and Characterization of the First Murine Model of Alzheimer's Disease with Mutated AβPP Inserted in a BALB/c Background (C.B6/J-APPswe).

Marta Balietti, Tiziana Casoli, Belinda Giorgetti, Roberto Colangeli, Cristina Nicoletti, Moreno Solazzi, Arianna Pugliese, Fiorenzo Conti

Open access · bronzeAbstract read
In one paragraph

Article in Journal of Alzheimer's disease : JAD, 2023. 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
0.2field-weighted citation impact, top 49% 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

1 citing paper in PubMed, 1 citations in OpenAlex.

  1. 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.

Marta BaliettiCenter for Neurobiology of Aging, IRCCS INRCA, Ancona, Italy.
Tiziana CasoliCenter for Neurobiology of Aging, IRCCS INRCA, Ancona, Italy.
Belinda GiorgettiCenter for Neurobiology of Aging, IRCCS INRCA, Ancona, Italy.
Roberto ColangeliSection of Neuroscience and Cell Biology, Department of Experimental and Clinical Medicine, Università Politecnica delle Marche, Ancona, Italy.
Cristina NicolettiSection of Neuroscience and Cell Biology, Department of Experimental and Clinical Medicine, Università Politecnica delle Marche, Ancona, Italy.
Moreno SolazziCenter for Neurobiology of Aging, IRCCS INRCA, Ancona, Italy.
Arianna PuglieseSection of Neuroscience and Cell Biology, Department of Experimental and Clinical Medicine, Università Politecnica delle Marche, Ancona, Italy.
Fiorenzo ContiCenter for Neurobiology of Aging, IRCCS INRCA, Ancona, Italy.
Istituto Nazionale di Riposo e Cura per Anziani · ITMarche Polytechnic University · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNumerous mouse models of Alzheimer's disease (AD) are available, but all suffer from certain limitations, thus prompting further attempts. To date, no one model exists with amyloidopathy in a BALB/c strain.

objectiveTo generate and characterize the C.B6/J-APPswe mouse, a model of AD with a mutated human gene for the amyloid-β protein precursor (AβPP) inserted in a BALB/c background.

methodsWe analyzed five groups at different ages (3, 6, 9, 12, and 16-18 months) of C.B6/J-APPswe and wild-type mice (50% males and 50% females) for the main hallmarks of AD by western blotting, amyloid-β (Aβ) ELISA, immunocytochemistry, electrophysiology, and behavioral tests.

resultsThe C.B6/J-APPswe mouse displays early AβPP and Aβ production, late amyloid plaques formation, high level of Tau phosphorylation, synaptic deficits (reduced density and functional impairment due to a reduced post-synaptic responsiveness), neurodegeneration caused by apoptosis and necroptosis/necrosis, microgliosis, astrocytic abnormalities, and sex-related differences in explorative behavior, anxiety-like behavior, and spatial long-term and working memories. Social housing is feasible despite the intra-cage aggressiveness of male animals.

conclusionC.B6/J-APPswe mice develop most of the distinctive features of AD and is a suitable model for the study of brain atrophy mechanisms and of the differences between males and females in the onset of cognitive/non-cognitive deficits.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAnimalsDisease Models, AnimalFemaleHumansMaleMiceMice, TransgenicAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAlzheimer’s diseaseamyloid-β protein precursorcognitive impairmentcongenic mouseneurodegenerationneuroinflammationsex-related differencessynaptic alteration

Identifiers

PMID37182890
PMCPMC10357192
OpenAlexW4376254977

What OpenQuestion holds

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Registered trials

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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.