Enrichment pathway analysis. The inflammatory genetic background in Bipolar Disorder

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Enrichment pathway analysis. The inflammatory genetic background in Bipolar Disorder. / Drago, Antonio; Crisafulli, Concetta; Calabrò, Marco; Serretti, Alessandro.

I: Journal of Affective Disorders, Bind 179, 01.07.2015, s. 88-94.

Publikation: Bidrag til tidsskrift/Konferencebidrag i tidsskrift /Bidrag til avisTidsskriftartikelForskningpeer review

Harvard

Drago, A, Crisafulli, C, Calabrò, M & Serretti, A 2015, 'Enrichment pathway analysis. The inflammatory genetic background in Bipolar Disorder', Journal of Affective Disorders, bind 179, s. 88-94. https://doi.org/10.1016/j.jad.2015.03.032

APA

Drago, A., Crisafulli, C., Calabrò, M., & Serretti, A. (2015). Enrichment pathway analysis. The inflammatory genetic background in Bipolar Disorder. Journal of Affective Disorders, 179, 88-94. https://doi.org/10.1016/j.jad.2015.03.032

CBE

Drago A, Crisafulli C, Calabrò M, Serretti A. 2015. Enrichment pathway analysis. The inflammatory genetic background in Bipolar Disorder. Journal of Affective Disorders. 179:88-94. https://doi.org/10.1016/j.jad.2015.03.032

MLA

Vancouver

Drago A, Crisafulli C, Calabrò M, Serretti A. Enrichment pathway analysis. The inflammatory genetic background in Bipolar Disorder. Journal of Affective Disorders. 2015 jul. 1;179:88-94. https://doi.org/10.1016/j.jad.2015.03.032

Author

Drago, Antonio ; Crisafulli, Concetta ; Calabrò, Marco ; Serretti, Alessandro. / Enrichment pathway analysis. The inflammatory genetic background in Bipolar Disorder. I: Journal of Affective Disorders. 2015 ; Bind 179. s. 88-94.

Bibtex

@article{23d786fb20584344bffb9ef415e93e06,
title = "Enrichment pathway analysis. The inflammatory genetic background in Bipolar Disorder",
abstract = "INTRODUCTION: The pathophysiology of Bipolar Disorder (BD) is yet to be fully characterized. In the last years attention was focused on neurodevelopment or neurodegenerative events. In this context, hyper- and hypo- activation of inflammatory cascades may play a role in modulating the architecture and function of neuronal tissues. In the present paper we tested the enrichment of molecular pathways related to inflammatory cascades (IL-1, IL-2, IL-6, IL-8, TNF and INF) testing whether genes related to these systems hold more variations associated with the risk for BD than expected.METHODS: ~7000 bipolar patients and controls with genome-wide data available from NIMH dataset were analyzed. SNPs were imputed, checked for quality control, pruned and tested for association (0.01RESULTS: As a result, IL-6, IL-8 and IFN related pathways held twice to thrice the number of expected variants associated with BD. These tests resisted the permutation analysis.LIMITATIONS: The restricted number of inflammatory components included in the analysis and the lack of functional consequences for some of the SNPs analyzed may be biased; however, these choices helped the authors to lighten the statistical computational load for the analyses and at the same time included possibly hidden SNPs in linkage disequilibrium with the analyzed variations.CONCLUSIONS: We bring evidence that the inflammatory cascades may be genetically varied in Bipolar patients. This genetic background may explain part of the pathophysiology of the disorder.",
keywords = "Bipolar Disorder, Case-Control Studies, Databases, Genetic, Female, Genetic Background, Genetic Predisposition to Disease, Genome-Wide Association Study, Humans, Inflammation, Inflammation Mediators, Male, Polymorphism, Single Nucleotide, Signal Transduction",
author = "Antonio Drago and Concetta Crisafulli and Marco Calabr{\`o} and Alessandro Serretti",
note = "Copyright {\textcopyright} 2015 Elsevier B.V. All rights reserved.",
year = "2015",
month = jul,
day = "1",
doi = "10.1016/j.jad.2015.03.032",
language = "English",
volume = "179",
pages = "88--94",
journal = "Journal of Affective Disorders",
issn = "0165-0327",
publisher = "Elsevier BV",

}

RIS

TY - JOUR

T1 - Enrichment pathway analysis. The inflammatory genetic background in Bipolar Disorder

AU - Drago, Antonio

AU - Crisafulli, Concetta

AU - Calabrò, Marco

AU - Serretti, Alessandro

N1 - Copyright © 2015 Elsevier B.V. All rights reserved.

PY - 2015/7/1

Y1 - 2015/7/1

N2 - INTRODUCTION: The pathophysiology of Bipolar Disorder (BD) is yet to be fully characterized. In the last years attention was focused on neurodevelopment or neurodegenerative events. In this context, hyper- and hypo- activation of inflammatory cascades may play a role in modulating the architecture and function of neuronal tissues. In the present paper we tested the enrichment of molecular pathways related to inflammatory cascades (IL-1, IL-2, IL-6, IL-8, TNF and INF) testing whether genes related to these systems hold more variations associated with the risk for BD than expected.METHODS: ~7000 bipolar patients and controls with genome-wide data available from NIMH dataset were analyzed. SNPs were imputed, checked for quality control, pruned and tested for association (0.01RESULTS: As a result, IL-6, IL-8 and IFN related pathways held twice to thrice the number of expected variants associated with BD. These tests resisted the permutation analysis.LIMITATIONS: The restricted number of inflammatory components included in the analysis and the lack of functional consequences for some of the SNPs analyzed may be biased; however, these choices helped the authors to lighten the statistical computational load for the analyses and at the same time included possibly hidden SNPs in linkage disequilibrium with the analyzed variations.CONCLUSIONS: We bring evidence that the inflammatory cascades may be genetically varied in Bipolar patients. This genetic background may explain part of the pathophysiology of the disorder.

AB - INTRODUCTION: The pathophysiology of Bipolar Disorder (BD) is yet to be fully characterized. In the last years attention was focused on neurodevelopment or neurodegenerative events. In this context, hyper- and hypo- activation of inflammatory cascades may play a role in modulating the architecture and function of neuronal tissues. In the present paper we tested the enrichment of molecular pathways related to inflammatory cascades (IL-1, IL-2, IL-6, IL-8, TNF and INF) testing whether genes related to these systems hold more variations associated with the risk for BD than expected.METHODS: ~7000 bipolar patients and controls with genome-wide data available from NIMH dataset were analyzed. SNPs were imputed, checked for quality control, pruned and tested for association (0.01RESULTS: As a result, IL-6, IL-8 and IFN related pathways held twice to thrice the number of expected variants associated with BD. These tests resisted the permutation analysis.LIMITATIONS: The restricted number of inflammatory components included in the analysis and the lack of functional consequences for some of the SNPs analyzed may be biased; however, these choices helped the authors to lighten the statistical computational load for the analyses and at the same time included possibly hidden SNPs in linkage disequilibrium with the analyzed variations.CONCLUSIONS: We bring evidence that the inflammatory cascades may be genetically varied in Bipolar patients. This genetic background may explain part of the pathophysiology of the disorder.

KW - Bipolar Disorder

KW - Case-Control Studies

KW - Databases, Genetic

KW - Female

KW - Genetic Background

KW - Genetic Predisposition to Disease

KW - Genome-Wide Association Study

KW - Humans

KW - Inflammation

KW - Inflammation Mediators

KW - Male

KW - Polymorphism, Single Nucleotide

KW - Signal Transduction

U2 - 10.1016/j.jad.2015.03.032

DO - 10.1016/j.jad.2015.03.032

M3 - Journal article

C2 - 25855618

VL - 179

SP - 88

EP - 94

JO - Journal of Affective Disorders

JF - Journal of Affective Disorders

SN - 0165-0327

ER -