Evidence map›Paper›PMID 29079292›Full record

ArticleNeuropharmacology2018

P2X receptor overexpression induced by soluble oligomers of amyloid beta peptide potentiates synaptic failure and neuronal dyshomeostasis in cellular models of Alzheimer's disease.

Francisco Sáez-Orellana, María C Fuentes-Fuentes, Pamela A Godoy, Tiare Silva-Grecchi, Jessica D Panes, Leonardo Guzmán, Gonzalo E Yévenes, Javiera Gavilán, Terrance M Egan, Luis G Aguayo and 1 more

Open access · greenAbstract read
In one paragraph

Article in Neuropharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.4field-weighted citation impact, top 8% 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

24 citing papers in PubMed, 43 citations in OpenAlex.

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  19. The Role of P2X7 Receptor in Alzheimer's Disease.Frontiers in molecular neuroscience · 2020
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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

11 authors at 2 institutions in 2 countries.

Francisco Sáez-OrellanaNeuroactive Compounds Screening Laboratory, Physiology Department, Biological Sciences Faculty, Universidad de Concepción, Concepción, Chile.
María C Fuentes-FuentesNeuroactive Compounds Screening Laboratory, Physiology Department, Biological Sciences Faculty, Universidad de Concepción, Concepción, Chile.
Pamela A GodoyNeuroactive Compounds Screening Laboratory, Physiology Department, Biological Sciences Faculty, Universidad de Concepción, Concepción, Chile.
Tiare Silva-GrecchiNeuroactive Compounds Screening Laboratory, Physiology Department, Biological Sciences Faculty, Universidad de Concepción, Concepción, Chile.
Jessica D PanesNeuroactive Compounds Screening Laboratory, Physiology Department, Biological Sciences Faculty, Universidad de Concepción, Concepción, Chile.
Leonardo GuzmánMolecular Neurobiology Laboratory, Physiology Department, Biological Sciences Faculty, Universidad de Concepción, Concepción, Chile.
Gonzalo E YévenesNeuropharmacology Laboratory, Physiology Department, Biological Sciences Faculty, Universidad de Concepción, Concepción, Chile.
Javiera GavilánNeuroactive Compounds Screening Laboratory, Physiology Department, Biological Sciences Faculty, Universidad de Concepción, Concepción, Chile.
Terrance M EganDepartment of Pharmacology and Physiology, School of Medicine, Saint Louis University, St. Louis, MO, USA.
Luis G AguayoNeuropharmacology Laboratory, Physiology Department, Biological Sciences Faculty, Universidad de Concepción, Concepción, Chile.
Jorge FuentealbaNeuroactive Compounds Screening Laboratory, Physiology Department, Biological Sciences Faculty, Universidad de Concepción, Concepción, Chile. Electronic address: jorgefuentealba@udec.cl.
University of Concepción · CLSaint Louis University · US

Funding

Gating and conduction of ATP-gated ion channelsR01GM070925 · NIGMS · SAINT LOUIS UNIVERSITY · PI EGAN, TERRANCE M · 2004 to 2007
$1.3M
Selective regulation of the calcium component of the ATP-gated P2X7 currentR01GM112188 · NIGMS · SAINT LOUIS UNIVERSITY · PI EGAN, TERRANCE M · 2016 to 2019
$1.2M
NIGMS NIH HHS R01 GM070925NIGMS NIH HHS R01 GM112188
6 · The paper itself

Abstract

The most common cause of dementia is Alzheimer's disease. The etiology of the disease is unknown, although considerable evidence suggests a critical role for the soluble oligomers of amyloid beta peptide (Aβ). Because Aβ increases the expression of purinergic receptors (P2XRs) in vitro and in vivo, we studied the functional correlation between long-term exposure to Aβ and the ability of P2XRs to modulate network synaptic tone. We used electrophysiological recordings and Ca

Indexed as

Adenosine TriphosphateAmyloid beta-PeptidesAnimalsCells, CulturedCell SurvivalCerebral CortexDisks Large Homolog 4 ProteinEmbryo, MammalianExcitatory Postsynaptic PotentialsFemaleMicrotubule-Associated ProteinsNeuronsNeurotransmitter AgentsPatch-Clamp TechniquesPeptide FragmentsPlatelet Aggregation InhibitorsAdenosine TriphosphateAmyloid beta-PeptidesDisks Large Homolog 4 ProteinDlg4 protein, ratMAP2 protein, ratMicrotubule-Associated ProteinsNeurotransmitter AgentsPeptide FragmentsPlatelet Aggregation InhibitorsPyridoxal Phosphatepyridoxal phosphate-6-azophenyl-2',4'-disulfonic acidReceptors, Purinergic P2XAlzheimer's diseaseAmyloid-β peptideATPP2X receptorSynaptic failure

Identifiers

PMID29079292
PMCPMC5858180
OpenAlexW2765960767

What OpenQuestion holds

Textmetadata
LicenceTDM
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.