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The role of IL18-607C > A and IL18-137G > C promoter polymorphisms in antidepressant treatment phenotypes: A preliminary report

Title
The role of IL18-607C > A and IL18-137G > C promoter polymorphisms in antidepressant treatment phenotypes: A preliminary report
Type
Article in International Scientific Journal
Year
2016
Authors
Santos, M
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Carvalho, S
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Mota Pereira, J
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Pimentel, P
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Maia, D
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Correia, D
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Gomes, S
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Cruz, A
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Rui Medeiros
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Journal
Title: Neuroscience LettersImported from Authenticus Search for Journal Publications
Vol. 622
Pages: 107-112
ISSN: 0304-3940
Publisher: Elsevier
Other information
Authenticus ID: P-00K-EYP
Abstract (EN): Recent studies suggest that immune activation and cytokines, such as IL-18, are involved in depression. IL-18 is expressed in brain and is increased in patients with moderate to severe depression. In this study we aim to evaluate the role of ILI 8-607C>A and 1L18-137G>C promoter polymorphisms in antidepressant treatment phenotypes, specifically relapse and treatment resistant depression (TRD). We genotyped the referred polymorphisms in a subset of 80 MDD patients followed at Hospital Magalhaes Lemos, Portugal, within a period of 27 months. Patients carrying IL18-607 CA or AA genotypes were significantly more prone to relapse after AD treatment and present a significantly lower time to relapse than patients carrying CC genotype. Similarly, patients carrying IL18-137 GC or CC genotypes have a significantly higher risk of relapse and display relapse significantly earlier than the ones carrying GG genotype. Due to the low number of IL18-607 CC and IL18-137 GG in the relapse subgroup (n = 3 and n = 5, respectively), results were validated by bootstrapping analysis, and remained significant. No association was found between the evaluated genetic polymorphisms and TRD.IL18 peripheral mRNA levels were upregulated in IL18-607 CA or AA carriers. This preliminary report indicates that IL18-607C>A and IL18-137G>C genetic polymorphisms seem to influence depression relapse after antidepressant treatment in our subset of depressed patients, and may possibly contribute to the disregulated IL-18 levels found in patients with depression.
Language: English
Type (Professor's evaluation): Scientific
No. of pages: 6
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