Evidence map›Paper›PMID 30607529›Full record

ArticleEuropean archives of psychiatry and clinical neuroscience2020

Analysis of KCNH2 and CACNA1C schizophrenia risk genes on EEG functional network modulation during an auditory odd-ball task.

Alba Lubeiro, Mar Fatjó-Vilas, Maria Guardiola, Carmen Almodóvar, Javier Gomez-Pilar, Benjamin Cea-Cañas, Jesús Poza, Aitor Palomino, Marta Gómez-García, Jone Zugasti and 1 more

Abstract read
PubMed Publisher
In one paragraph

Article in European archives of psychiatry and clinical neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 18% 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

5 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Analysis ofGenes · 2022
    Article
  4. Article
  5. Article
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 5 institutions in 2 countries.

Alba LubeiroPsychiatry Department, School of Medicine, University of Valladolid, Av. Ramón y Cajal, 7, 47005, Valladolid, Spain. alba.lubeiro@gmail.com.ORCID http://orcid.org/0000-0003-4990-5014
Mar Fatjó-VilasFIDMAG Germanes Hospitalàries Research Foundation, Carrer Del Dr. Antoni Pujadas, 38 Sant Boi De Llobregat, 08830, Barcelona, Spain. mfatjo-vilas@fidmag.com.
Maria GuardiolaFIDMAG Germanes Hospitalàries Research Foundation, Carrer Del Dr. Antoni Pujadas, 38 Sant Boi De Llobregat, 08830, Barcelona, Spain.
Carmen AlmodóvarFIDMAG Germanes Hospitalàries Research Foundation, Carrer Del Dr. Antoni Pujadas, 38 Sant Boi De Llobregat, 08830, Barcelona, Spain.
Javier Gomez-PilarBiomedical Engineering Group, Department TSCIT, ETS Ingenieros de Telecomunicación, University of Valladolid, Valladolid, Spain.
Benjamin Cea-CañasNeurophysiology service, University Hospital of Valladolid, Valladolid, Spain.
Jesús PozaBiomedical Engineering Group, Department TSCIT, ETS Ingenieros de Telecomunicación, University of Valladolid, Valladolid, Spain.
Aitor PalominoAchucarro Basque Center for Neurosciences, CIBERNED and Departamento de Neurociencias, Universidad del País Vasco, Leioa, Spain.
Marta Gómez-GarcíaPsychiatry service, University Hospital of Valladolid, Valladolid, Spain.
Jone ZugastiPsychiatry Department, University Hospital of Álava, Álava, Spain.
Vicente MolinaPsychiatry Department, School of Medicine, University of Valladolid, Av. Ramón y Cajal, 7, 47005, Valladolid, Spain.
Universidad de Valladolid · ESInstituto de Salud Carlos III · ESHospital Mare de Déu de la Mercè · ESHospital Universitario Araba · ESUniversity of the Basque Country · ES

Funding

NATURAL AND SYNTHETIC ANALGESICS AND NOVEL CYTOTOXIC AGEK04CA001134 · NCI · PURDUE UNIVERSITY WEST LAFAYETTE · PI BOGER, DALE L · 1985 to 1987
–
Comissionat per a Universitats i Recerca del DIUE 2017SGR1271Consejería de Educación, Junta de Castilla y León VA037U16Consejería de Educación, Junta de Castilla y León VA059U13Gerencia Regional de Salud de Castilla y León GRS 1134/A/15Gerencia Regional de Salud de Castilla y León GRS 932/A/14Instituto de Salud Carlos III PI11/02203Instituto de Salud Carlos III PI11/02708Instituto de Salud Carlos III PI15/00299Instituto de Salud Carlos III PI15/01420Interreg 0378_AD_EEGWA_2_P
6 · The paper itself

Abstract

A deficit in task-related functional connectivity modulation from electroencephalogram (EEG) has been described in schizophrenia. The use of measures of neuronal connectivity as an intermediate phenotype may allow identifying genetic factors involved in these deficits, and therefore, establishing underlying pathophysiological mechanisms. Genes involved in neuronal excitability and previously associated with the risk for schizophrenia may be adequate candidates in relation to functional connectivity alterations in schizophrenia. The objective was to study the association of two genes of voltage-gated ion channels (CACNA1C and KCNH2) with the functional modulation of the cortical networks measured with EEG and graph-theory parameter during a cognitive task, both in individuals with schizophrenia and healthy controls. Both CACNA1C (rs1006737) and KCNH2 (rs3800779) were genotyped in 101 controls and 50 schizophrenia patients. Small-world index (SW) was calculated from EEG recorded during an odd-ball task in two different temporal windows (pre-stimulus and response). Modulation was defined as the difference in SW between both windows. Genetic, group and their interaction effects on SW in the pre-stimulus window and in modulation were evaluated using ANOVA. The CACNA1C genotype was not associated with SW properties. KCNH2 was significantly associated with SW modulation. Healthy subjects showed a positive SW modulation irrespective of the KCNH2 genotype, whereas within patients allele-related differences were observed. Patients carrying the KCNH2 risk allele (A) presented a negative SW modulation and non-carriers showed SW modulation similar to the healthy subjects. Our data suggest that KCNH2 genotype contributes to the efficient modulation of brain electrophysiological activity during a cognitive task in schizophrenia patients.

Indexed as

ConnectomeAdultAttentionAuditory PerceptionCalcium Channels, L-TypeCerebral CortexElectroencephalographyERG1 Potassium ChannelFemaleGenotypeHumansMaleNerve NetPolymorphism, Single NucleotideRiskSchizophreniaCACNA1C protein, humanCalcium Channels, L-TypeERG1 Potassium ChannelKCNH2 protein, humanCACNA1CElectroencephalographyKCNH2SchizophreniaSmall-world

Identifiers

PMID30607529
OpenAlexW2907581023

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.