Evidence map›Paper›PMID 31829002›Full record

ArticleJournal of psychiatry & neuroscience : JPN2019

CACNA1C polymorphism and brain cortical structure in bipolar disorder

Erik Smedler, Christoph Abé, Erik Pålsson, Martin Ingvar, Mikael Landén

Open access · diamondAbstract read
In one paragraph

Article in Journal of psychiatry & neuroscience : JPN, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

11 citing papers in PubMed, 17 citations in OpenAlex.

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  6. Cortical morphological heterogeneity of schizophrenia and its relationship with glutamatergic receptor variations.European psychiatry : the journal of the Association of European Psychiatrists · 2023
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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

5 authors at 2 institutions in 1 country.

Erik SmedlerFrom the Department of Psychiatry and Neurochemistry, Sahlgrenska Academy at Gothenburg University, Gothenburg, Sweden (Smedler, Pålsson, Landén); the Department of Clinical Neuroscience, Osher Center for Integrative Medicine, Karolinska Institutet, Stockholm, Sweden (Abé, Ingvar); and the Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden (Landén).
Christoph AbéFrom the Department of Psychiatry and Neurochemistry, Sahlgrenska Academy at Gothenburg University, Gothenburg, Sweden (Smedler, Pålsson, Landén); the Department of Clinical Neuroscience, Osher Center for Integrative Medicine, Karolinska Institutet, Stockholm, Sweden (Abé, Ingvar); and the Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden (Landén).
Erik PålssonFrom the Department of Psychiatry and Neurochemistry, Sahlgrenska Academy at Gothenburg University, Gothenburg, Sweden (Smedler, Pålsson, Landén); the Department of Clinical Neuroscience, Osher Center for Integrative Medicine, Karolinska Institutet, Stockholm, Sweden (Abé, Ingvar); and the Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden (Landén).
Martin IngvarFrom the Department of Psychiatry and Neurochemistry, Sahlgrenska Academy at Gothenburg University, Gothenburg, Sweden (Smedler, Pålsson, Landén); the Department of Clinical Neuroscience, Osher Center for Integrative Medicine, Karolinska Institutet, Stockholm, Sweden (Abé, Ingvar); and the Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden (Landén).
Mikael LandénFrom the Department of Psychiatry and Neurochemistry, Sahlgrenska Academy at Gothenburg University, Gothenburg, Sweden (Smedler, Pålsson, Landén); the Department of Clinical Neuroscience, Osher Center for Integrative Medicine, Karolinska Institutet, Stockholm, Sweden (Abé, Ingvar); and the Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden (Landén).
Karolinska Institutet · SEUniversity of Gothenburg · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: The CACNA1C gene encodes the 1C subunit of L-type voltage-gated calcium channels and has been associated with several psychiatric syndromes — including bipolar disorder — in several genome-wide association studies. Experimental and clinical studies have reported changes with respect to behaviour and biomarkers in risk allele carriers, corroborating the essential role of the CACNA1C gene in neurons, during development and in the mature brain. However, the association of this gene with regional cortical thickness has not been evaluated in patients with bipolar disorder. Methods: Using magnetic resonance imaging, we measured the average cortical thickness of 68 brain regions in 87 patients genotyped for the single-nucleotide polymorphism rs1006737 in CACNA1C. Results: We found associations with the mean thickness of several cortical areas: the left lateral orbitofrontal and rostral anterior cingulate cortices, as well as other parts of the frontal and parietal cortices. Limitations: This cross-sectional cohort study could not fully differentiate correlation from causation. Conclusion: The CACNA1C polymorphism rs1006737 is associated with the mean thickness of cortical brain areas that have been shown to be altered in bipolar disorder.

Indexed as

Magnetic Resonance ImagingAdultBipolar DisorderCalcium Channels, L-TypeCerebral CortexCross-Sectional StudiesFemaleHumansMaleMiddle AgedPolymorphism, GeneticCACNA1C protein, humanCalcium Channels, L-Type

Identifiers

PMID31829002
PMCPMC7828982
OpenAlexW3004354393

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.