Evidence map›Paper›PMID 28237964›Full record

ArticleDisease models & mechanisms2017

Vulnerability of primary neurons derived from Tg2576 Alzheimer mice to oxygen and glucose deprivation: role of intraneuronal amyloid-β accumulation and astrocytes.

Vito Antonio Baldassarro, Alessandra Marchesini, Luciana Giardino, Laura Calzà

Open access · goldAbstract read
In one paragraph

Article in Disease models & mechanisms, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

20 citing papers in PubMed, 26 citations in OpenAlex.

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  8. Review
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  12. White Matter and Neuroprotection in Alzheimer's Dementia.Molecules (Basel, Switzerland) · 2020
    Review
  13. Oxidative Stress in Alzheimer's Disease:Oxidative medicine and cellular longevity · 2020
    Article
  14. Article
  15. Amyloid β-Induced Upregulation of NaScientific reports · 2019
    Article
  16. Article
  17. Article
  18. Article
  19. Article
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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

4 authors at 2 institutions in 1 country.

Vito Antonio BaldassarroInterdepartmental Centre for Industrial Research in Health Science and Technologies (ICIR - HST), University of Bologna, 40064 Ozzano Emilia, Bologna, Italy.ORCID 0000-0003-1020-4261
Alessandra MarchesiniFondazione IRET, 40064 Ozzano Emilia, Bologna, Italy.ORCID 0000-0002-5834-7117
Luciana GiardinoInterdepartmental Centre for Industrial Research in Health Science and Technologies (ICIR - HST), University of Bologna, 40064 Ozzano Emilia, Bologna, Italy.ORCID 0000-0003-3107-3264
Laura CalzàInterdepartmental Centre for Industrial Research in Health Science and Technologies (ICIR - HST), University of Bologna, 40064 Ozzano Emilia, Bologna, Italy laura.calza@unibo.it.
Fondazione IRET ONLUS · ITUniversity of Bologna · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Microvascular dysfunction is considered an integral part of Alzheimer disease (AD) pathogenesis, but the possible relationship between amyloid pathology, microvascular dysfunction and cell death is still unclear. In order to investigate the influence of intraneuronal amyloid-β (Aβ) accumulation on vulnerability to hypoxia, we isolated primary cortical neurons from Tg2576 (carrying the amyloid precursor protein APPSwe mutation) and wild-type fetal mice. We first demonstrated that neurons isolated from Tg2576 newborn mice show an increase in VEGFa mRNA expression and a decrease in the expression of the two VEGF receptors, Flt1 and Kdr, compared with wild-type cells. Moreover, APPSwe primary neurons displayed higher spontaneous and glutamate-induced cell death. We then deprived the cultures of oxygen and glucose (OGD) as an

Indexed as

Amyloid beta-PeptidesAmyloid Precursor Protein SecretasesAnimalsAnimals, NewbornAstrocytesCells, CulturedCulture Media, ConditionedGlucoseMiceMice, TransgenicNeuronsOxygenAmyloid beta-PeptidesAmyloid Precursor Protein SecretasesCulture Media, ConditionedGlucoseOxygenAlzheimer's diseaseGlutamateIntraneuronal amyloidNeurovascular couplingOxygen glucose deprivationPrimary neurons

Identifiers

PMID28237964
PMCPMC5451168
OpenAlexW2589493479

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.