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P01-89 - Preliminary Analysis of the Functional Consequences of the CACNA1C Gene Polymorphism on Emotional Processing in Bipolar Disorder

Published online by Cambridge University Press:  17 April 2020

G. Ruberto
Affiliation:
Section of Neurobiology of Psychosis, Institute of Psychiatry, King's College, London, UK Department of Psychiatry, Sapienza University, Second Medical School, Sant’ Andrea Hospital, Rome, Italy
G. Lelli-Chiesa
Affiliation:
Section of Neurobiology of Psychosis, Institute of Psychiatry, King's College, London, UK Department of Psychiatry, Sapienza University, Second Medical School, Sant’ Andrea Hospital, Rome, Italy
E. Vassos
Affiliation:
Social, Genetic & Developmental Psychiatry Centre, Institute of Psychiatry, King's College, London, UK
M. Maierú
Affiliation:
Social, Genetic & Developmental Psychiatry Centre, Institute of Psychiatry, King's College, London, UK
R. Tatarelli
Affiliation:
Department of Psychiatry, Sapienza University, Second Medical School, Sant’ Andrea Hospital, Rome, Italy
P. Girardi
Affiliation:
Department of Psychiatry, Sapienza University, Second Medical School, Sant’ Andrea Hospital, Rome, Italy
D. Collier
Affiliation:
Social, Genetic & Developmental Psychiatry Centre, Institute of Psychiatry, King's College, London, UK
M.J. Kempton
Affiliation:
Section of Neurobiology of Psychosis, Institute of Psychiatry, King's College, London, UK
S. Frangou
Affiliation:
Section of Neurobiology of Psychosis, Institute of Psychiatry, King's College, London, UK

Abstract

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Objectives

A single nucleotide polymorphism within the CACNA1C gene (rs1006737) has been found to confer increased risk of Bipolar Disorder (BD) and has been linked to altered neuronal gating and emotional behaviour. As current models of BD suggest abnormal integration within frontolimbic networks, our aim was to explore the effect of the CACNA1C genotype on prefrontal and limbic activation.

Methods

We genotyped 90 participants from the Vulnerability to Bipolar Disorder Study comprising of 41 euthymic BD patients and 49 healthy controls. Functional magnetic resonance imaging data were obtained while participants performed a fearful versus neutral facial affect processing task.

Results

We found a significant diagnosis by genotype interaction with BD patients homozygous for the risk allele having reduced prefrontal activation compared to the other groups.

Conclusions

The present findings support the hypothesis that the rs1006737 polymorphism in the CACNA1C gene confers increased risk of BD by modulating amygdala and PFC activation during emotional processing.

Type
Affective disorders / Unipolar depression / Bipolar disorder
Copyright
Copyright © European Psychiatric Association 2010
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