Glutamate cysteine ligase (GCL) and self reported depression: an association study from the HUNT

Berk, Michael, Johansson, Stefan, Wray, Naomi R., Williams, Lana, Olsson, Craig, Haavik, Jan and Bjerkeset, Ottar (2011) Glutamate cysteine ligase (GCL) and self reported depression: an association study from the HUNT. Journal of Affective Disorders, 131 1-3: 207-213. doi:10.1016/j.jad.2010.12.019


Author Berk, Michael
Johansson, Stefan
Wray, Naomi R.
Williams, Lana
Olsson, Craig
Haavik, Jan
Bjerkeset, Ottar
Title Glutamate cysteine ligase (GCL) and self reported depression: an association study from the HUNT
Journal name Journal of Affective Disorders   Check publisher's open access policy
ISSN 0165-0327
1573-2517
Publication date 2011
Sub-type Article (original research)
DOI 10.1016/j.jad.2010.12.019
Open Access Status
Volume 131
Issue 1-3
Start page 207
End page 213
Total pages 7
Place of publication Amsterdam, Netherlands
Publisher Elsevier
Language eng
Formatted abstract
Background: There is increasing evidence suggesting oxidative stress may play a role in the aetiology of depression. Glutathione is the brain's predominant free radical scavenger, and associated polymorphisms of the glutamate cysteine ligase (GCL) gene have been reported for related psychiatric disorders. The aim of the study was to investigate candidate polymorphisms of GCL validated in schizophrenia and their association with current state depression, as measured by the Hospital Anxiety and Depression Scale (HADS).

Methods: Polymorphisms were genotyped on 983 cases and 967 controls selected from a population sample of adults participating in the Nord-Trøndelag Health Study. Cases were the top scoring individuals (98.5th percentile) on the HADS depression subscale while the controls were randomly selected from below this cut-off. The polymorphisms comprised three SNPs from GCLM, the gene encoding the GCL modifier and 9 SNPs plus a trinucleotide repeat (TNTR) from intron 1 and the 5′UTR of GCLC, the gene encoding the GCL catalytic subunit. Using the linkage disequilibrium between the GCLC markers we also tested whether SNPs could represent the variation of the TNTR.

Results: The candidate polymorphisms showed no evidence for association with depression. The C allele of SNP rs9474592 is coupled with the 9 GAG repeats allele of the TNTR, r2 = 0.81. None of the other SNPs either individually or as two or three-SNP haplotypes was associated with the TNTR alleles.

Limitations: Depression was self-reported and measured at one time point. Conclusions: This study provides no evidence to suggest that polymorphisms of GCL are associated with self-reported depression.
Keyword Oxidative stress
Glutamate cysteine ligase
Depression
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Non-UQ

Document type: Journal Article
Sub-type: Article (original research)
Collection: Queensland Brain Institute Publications
 
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Created: Thu, 23 Oct 2014, 16:19:16 EST by Debra McMurtrie on behalf of Queensland Brain Institute