Evidence map›Paper›PMID 26048451›Full record

ArticleEuropean archives of psychiatry and clinical neuroscience2016

CACNA1C risk variant is associated with increased amygdala volume.

T M Lancaster, S Foley, K E Tansey, D E J Linden, X Caseras

Abstract read
PubMed Publisher
In one paragraph

Article in European archives of psychiatry and clinical neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.2field-weighted citation impact, top 19% 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

13 citing papers in PubMed, 20 citations in OpenAlex.

  1. The Impact of Overexpression of the Mouse Ortholog ofBiological psychiatry global open science · 2025
    Article
  2. Article
  3. Article
  4. CACNA1C-Related Channelopathies.Handbook of experimental pharmacology · 2023
    Review
  5. Review
  6. Article
  7. Article
  8. Neuropsychiatric disease and treatment · 2020
    Article
  9. CACNA1C polymorphism and brain cortical structure in bipolar disorderJournal of psychiatry & neuroscience : JPN · 2019
    Article
  10. Article
  11. Review
  12. Alcohol Dependence Disrupts Amygdalar L-Type Voltage-Gated Calcium Channel Mechanisms.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
    Article
  13. 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

5 authors at 1 institution in 1 country.

T M LancasterNeuroscience and Mental Health Research Institute, Cardiff University, Hadyn Ellis Building, Maindy Road, Cardiff, Wales, UK. LancasterTM@cardiff.ac.uk.
S FoleyCardiff University Brain Research Imaging Centre (CUBRIC), School of Psychology, Cardiff University, 70 Park Place, Cardiff, CF10 3AT, Wales, UK.
K E TanseyMRC Centre for Neuropsychiatric Genetics and Genomics, Institute of Psychological Medicine and Clinical Neurosciences, Cardiff School of Medicine, Cardiff University, Cardiff, Wales, UK.
D E J LindenNeuroscience and Mental Health Research Institute, Cardiff University, Hadyn Ellis Building, Maindy Road, Cardiff, Wales, UK.
X CaserasCardiff University Brain Research Imaging Centre (CUBRIC), School of Psychology, Cardiff University, 70 Park Place, Cardiff, CF10 3AT, Wales, UK.
Cardiff University · GB

Funding

Medical Research Council G0800509Medical Research Council MR/K004360/1Medical Research Council MR/L010305/1
6 · The paper itself

Abstract

Genome-wide association studies suggest that genetic variation within L-type calcium channel subunits confer risk to psychosis. The single nucleotide polymorphism at rs1006737 in CACNA1C has been associated with both schizophrenia and bipolar disorder and with several intermediate phenotypes that may serve as neurobiological antecedents, linking psychosis to genetic aetiology. Amongst others, it has been implicated in alterations in amygdala structure and function. In the present study, we show that the risk allele (A) is associated with increased amygdala volume in healthy individuals (n = 258). This observation reinforces a hypothesis that genetic variation may confer risk to psychosis via alterations in limbic structures. Further study of CACNA1C using intermediate phenotypes for psychosis will determine the mechanisms by which variation in this gene confers risk.

Indexed as

AllelesAmygdalaCalcium Channels, L-TypeFemaleGenetic Association StudiesGenetic Predisposition to DiseaseHumansMaleOrgan SizePsychotic DisordersRisk FactorsYoung AdultCACNA1C protein, humanCalcium Channels, L-TypeAmygdalaBipolarCACNA1Crs1006737

Identifiers

PMID26048451
OpenAlexW600873163

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.