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Association of genetic variants of Glutamate Metabotropic Receptor 5 gene and state-anhedonia

Published online by Cambridge University Press:  01 September 2022

D. Török ,
X. Gonda ,
Z. Gal ,
N. Eszlari ,
G. Bagdy ,
G. Juhasz  and
P. Petschner
D. Török
Affiliation:
Semmelweis University, Department Of Pharmacodynamics, Budapest, Hungary
X. Gonda*
Affiliation:
Semmelweis University, Department Of Psychiatry And Psychotherapy, Budapest, Hungary NAP-2-SE New Antidepressant Target Research Group, Hungarian Brain Research Program, Semmelweis University, Budapest, Hungary
Z. Gal
Affiliation:
Semmelweis University, Department Of Pharmacodynamics, Budapest, Hungary
N. Eszlari
Affiliation:
Semmelweis University, Department Of Pharmacodynamics, Budapest, Hungary NAP-2-SE New Antidepressant Target Research Group, Hungarian Brain Research Program, Semmelweis University, Budapest, Hungary
G. Bagdy
Affiliation:
Semmelweis University, Department Of Pharmacodynamics, Budapest, Hungary NAP-2-SE New Antidepressant Target Research Group, Hungarian Brain Research Program, Semmelweis University, Budapest, Hungary
G. Juhasz
Affiliation:
Semmelweis University, Department Of Pharmacodynamics, Budapest, Hungary SE-NAP-2 Genetic Brain Imaging Migraine Research Group, Semmelweis University, Budapest, Hungary
P. Petschner
Affiliation:
Semmelweis University, Department Of Pharmacodynamics, Budapest, Hungary NAP-2-SE New Antidepressant Target Research Group, Hungarian Brain Research Program, Semmelweis University, Budapest, Hungary Institute of Chemical Research Kyoto University, Bioinformatics Center, Uji, Japan
*
*Corresponding author.

Abstract

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Introduction

Andedonia is one of the core symptoms of depression. It is known that in case of depressed individuals experiencing anhedonia, the classical antidepressants are often ineffective, thus investigation of this symptom would be essential. Recent studies highlight the possible role of the glutamatergic system in anhedonia however, the genetic background of these assumptions is still unclear.

Objectives

Our goal was to investigate the possible associations between state-anhedonia and genetic variants from GRM5 (Glutamate Metabotropic Receptor 5) gene.

Methods

For our analysis we used data from the NewMood (New Molecules in Mood Disorders, LSHM-CT-2004-503474) project. Participants (n = 1820) aged between 18-60, were recruited in Budapest and in Manchester. All volunteers filled out mental-health questionnaires and provided DNA sample. Genotyping was performed by Illumina’s CoreExom PsychChip. Altogether 1282 variants from GRM5 gene survived the genetic quality control steps. State-anhedonia was measured with an item from the Brief Symptom Inventory questionnaire. We performed logistic regression using Plink 2.0. During our analyses, age, gender, population and the top10 principal components of the genome were added into the model as covariates. Correction for linkage-disequilibrium were performed with LDlink.

Results

After the correction of linkage-disequilibrium, three independent variables (r2<0.2), (rs1827603, rs6483520, rs35669869) yielded significant (p<0.05) results, both in additive and in dominant model. In case of recessive model, only rs11020880 showed significant (p<0.05) effect.

Conclusions

The detected nominally significant associations between state-anhedonia and genetic variants from GRM5 gene strengthen previous assumptions about the possible relationship between glutamatergic system and anhedonia.

Disclosure

This study was supported by: MTA-SE Neuropsychopharmacology and Neurochemistry Research Group; 2017-1.2.1-NKP-2017-00002; KTIA_13_NAPA-II/14; KTIA_NAP_13-1-2013- 0001; KTIA_NAP_13-2- 2015-0001; 2020-4.1.1.-TKP2020 and 2019-2.1.7-ERA-NET-2020-00005 (TRAJEC

Keywords

GlutamateGRM5Geneticsanhedonia
Type
Abstract
Information
European Psychiatry , Volume 65 , Special Issue S1: Abstracts of the 30th European Congress of Psychiatry , June 2022 , pp. S148
Creative Commons
Creative Common License - CCCreative Common License - BY
This is an Open Access article, distributed under the terms of the Creative Commons Attribution licence (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted re-use, distribution, and reproduction in any medium, provided the original work is properly cited.
Copyright
© The Author(s), 2022. Published by Cambridge University Press on behalf of the European Psychiatric Association
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