A molecular pathway analysis stresses the role of inflammation and oxidative stress towards cognition in schizophrenia

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A molecular pathway analysis stresses the role of inflammation and oxidative stress towards cognition in schizophrenia. / Fischer, Ellen Kure; Drago, Antonio.

I: Journal of neural transmission (Vienna, Austria : 1996), Bind 124, Nr. 7, 07.2017, s. 765–774.

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

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Fischer, Ellen Kure ; Drago, Antonio. / A molecular pathway analysis stresses the role of inflammation and oxidative stress towards cognition in schizophrenia. I: Journal of neural transmission (Vienna, Austria : 1996). 2017 ; Bind 124, Nr. 7. s. 765–774.

Bibtex

@article{3e906f278816420d96397805453acc21,
title = "A molecular pathway analysis stresses the role of inflammation and oxidative stress towards cognition in schizophrenia",
abstract = "Cognitive processes have a genetic component and are impaired in Schizophrenia (SKZ). The exact nature of such impairment escapes definition. The aim of the present contribution was the identification of the molecular pathways enriched with mutations (SNPs) associated with cognitive performance during antipsychotic treatment. 765 individuals from the CATIE study, males = 559, mean age 40.93 ± 11.03 were included. Working memory and the verbal memory were the evaluated outcomes. A mixed regression model for repeated measures served in R for clinical and molecular pathway analysis. The analysis of quality was conducted under the following criteria: minor allele frequency >0.01, genotype call rate >95%, missing data frequency <5%, Hardy-Weimberg equilibrium threshold >0.0001. The inflation factor was controlled by lambda values. Input for the pathway analysis was SNPs at a p level <0.05 of association genome-wide. Gender, age, education and the duration of the disease were the clinical and socio-demographic variables associated with the cognitive performance. 4268977 SNPs were available after imputation and quality analysis. Pathways related to inflammation and oxidation were the most strongly associated with verbal memory and working memory at a conservative adjusted p value < 0.01. We report that inflammation and in particular the pathway associated with arachidonic acid was enriched in mutations associated with poorer performance at the verbal memory and working memory tasks in SKZ patients.",
keywords = "Journal Article",
author = "Fischer, {Ellen Kure} and Antonio Drago",
year = "2017",
month = jul,
doi = "10.1007/s00702-017-1730-y",
language = "English",
volume = "124",
pages = "765–774",
journal = "Journal of Neural Transmission",
issn = "0300-9564",
publisher = "Springer Wien",
number = "7",

}

RIS

TY - JOUR

T1 - A molecular pathway analysis stresses the role of inflammation and oxidative stress towards cognition in schizophrenia

AU - Fischer, Ellen Kure

AU - Drago, Antonio

PY - 2017/7

Y1 - 2017/7

N2 - Cognitive processes have a genetic component and are impaired in Schizophrenia (SKZ). The exact nature of such impairment escapes definition. The aim of the present contribution was the identification of the molecular pathways enriched with mutations (SNPs) associated with cognitive performance during antipsychotic treatment. 765 individuals from the CATIE study, males = 559, mean age 40.93 ± 11.03 were included. Working memory and the verbal memory were the evaluated outcomes. A mixed regression model for repeated measures served in R for clinical and molecular pathway analysis. The analysis of quality was conducted under the following criteria: minor allele frequency >0.01, genotype call rate >95%, missing data frequency <5%, Hardy-Weimberg equilibrium threshold >0.0001. The inflation factor was controlled by lambda values. Input for the pathway analysis was SNPs at a p level <0.05 of association genome-wide. Gender, age, education and the duration of the disease were the clinical and socio-demographic variables associated with the cognitive performance. 4268977 SNPs were available after imputation and quality analysis. Pathways related to inflammation and oxidation were the most strongly associated with verbal memory and working memory at a conservative adjusted p value < 0.01. We report that inflammation and in particular the pathway associated with arachidonic acid was enriched in mutations associated with poorer performance at the verbal memory and working memory tasks in SKZ patients.

AB - Cognitive processes have a genetic component and are impaired in Schizophrenia (SKZ). The exact nature of such impairment escapes definition. The aim of the present contribution was the identification of the molecular pathways enriched with mutations (SNPs) associated with cognitive performance during antipsychotic treatment. 765 individuals from the CATIE study, males = 559, mean age 40.93 ± 11.03 were included. Working memory and the verbal memory were the evaluated outcomes. A mixed regression model for repeated measures served in R for clinical and molecular pathway analysis. The analysis of quality was conducted under the following criteria: minor allele frequency >0.01, genotype call rate >95%, missing data frequency <5%, Hardy-Weimberg equilibrium threshold >0.0001. The inflation factor was controlled by lambda values. Input for the pathway analysis was SNPs at a p level <0.05 of association genome-wide. Gender, age, education and the duration of the disease were the clinical and socio-demographic variables associated with the cognitive performance. 4268977 SNPs were available after imputation and quality analysis. Pathways related to inflammation and oxidation were the most strongly associated with verbal memory and working memory at a conservative adjusted p value < 0.01. We report that inflammation and in particular the pathway associated with arachidonic acid was enriched in mutations associated with poorer performance at the verbal memory and working memory tasks in SKZ patients.

KW - Journal Article

U2 - 10.1007/s00702-017-1730-y

DO - 10.1007/s00702-017-1730-y

M3 - Journal article

C2 - 28477285

VL - 124

SP - 765

EP - 774

JO - Journal of Neural Transmission

JF - Journal of Neural Transmission

SN - 0300-9564

IS - 7

ER -