Skip header and navigation

Refine By

45 records – page 1 of 5.

Alcohol use disorders are associated with increased affective lability in bipolar disorder.

https://arctichealth.org/en/permalink/ahliterature287319
Source
J Affect Disord. 2017 Jan 15;208:316-324
Publication Type
Article
Date
Jan-15-2017
Author
Trine Vik Lagerberg
Sofie Ragnhild Aminoff
Monica Aas
Thomas Bjella
Chantal Henry
Marion Leboyer
Geir Pedersen
Frank Bellivier
Romain Icick
Ole A Andreassen
Bruno Etain
Ingrid Melle
Source
J Affect Disord. 2017 Jan 15;208:316-324
Date
Jan-15-2017
Language
English
Publication Type
Article
Keywords
Adult
Affect
Alcohol-Related Disorders - epidemiology
Bipolar Disorder - epidemiology
Comorbidity
Female
France - epidemiology
Humans
Male
Middle Aged
Norway - epidemiology
Substance-Related Disorders - epidemiology
Tobacco smoking
Young Adult
Abstract
Affective dysregulation is a core feature of bipolar disorder (BD), and inter-episodic affect lability is associated with more severe outcomes including comorbidity. Rates of daily tobacco smoking and substance use disorders in BD are high. Knowledge regarding relationships between affective lability and abuse of the most commonly used substances such as tobacco, alcohol and cannabis in BD is limited.
We investigated whether dimensions of inter-episodic affective lability as measured with the Affective Lability Scale - short form (ALS-SF) were associated with lifetime daily tobacco use or alcohol (AUD) or cannabis use disorders (CUD) in a sample of 372 French and Norwegian patients with BD I and II.
ALS-SF total score and all sub-dimensions (anxiety-depression, depression-elation and anger) were significantly associated with AUD, while only the depression-elation sub-dimension was associated with CUD, after controlling for possible confounders such as gender, age at interview, age at illness onset, BD subtype, duration of illness and other substance use disorders. Daily tobacco smoking was not significantly associated with affective lability.
Data for recent substance use or psychiatric comorbidities such as personality or hyperkinetic disorders were not available, and could have mediated the relationships.
AUD is associated with several dimensions of inter-episodic affective lability in BD, while CUD is associated with increased oscillations between depression and elation only. Increased affective lability may partly explain the increased illness severity of patients with BD and AUD or CUD. Affective lability should be treated in order to prevent these comorbidities.
PubMed ID
27810713 View in PubMed
Less detail

Association analysis of ANK3 gene variants in nordic bipolar disorder and schizophrenia case-control samples.

https://arctichealth.org/en/permalink/ahliterature130741
Source
Am J Med Genet B Neuropsychiatr Genet. 2011 Dec;156B(8):969-74
Publication Type
Article
Date
Dec-2011
Author
Martin Tesli
Pernille Koefoed
Lavinia Athanasiu
Morten Mattingsdal
Omar Gustafsson
Ingrid Agartz
Lars M Rimol
Andrew Brown
Katrine V Wirgenes
Lisa-Lena Smorr
Anna K Kähler
Thomas Werge
Ole Mors
Erling Mellerup
Erik G Jönsson
Ingrid Melle
Gunnar Morken
Srdjan Djurovic
Ole A Andreassen
Author Affiliation
Institute of Clinical Medicine, University of Oslo, Oslo, Norway. m.s.tesli@medisin.uio.no
Source
Am J Med Genet B Neuropsychiatr Genet. 2011 Dec;156B(8):969-74
Date
Dec-2011
Language
English
Publication Type
Article
Keywords
Ankyrins - genetics
Bipolar Disorder - genetics
Case-Control Studies
Female
Gene Frequency
Genetic Association Studies
Genetic Predisposition to Disease
Genetic Variation
Genotype
Humans
Iceland
Male
Polymorphism, Single Nucleotide
Scandinavia
Schizophrenia - genetics
Abstract
Genetic variants in ankyrin 3 (ANK3) have recently been shown to be associated with bipolar disorder (BD). We genotyped three ANK3 SNPs previously found to be associated with BD (rs10994336, rs1938526, and rs9804190) in a Scandinavian BD case-control sample (N = 854/2,614). Due to evidence of genetic overlap between BD and schizophrenia (SZ), we also genotyped these three SNPs in a Scandinavian SZ case-control sample (N = 1,073/2,919). Combining our Scandinavian samples with an Icelandic sample (N = 435 BD cases, 651 SZ cases, and 11,491 healthy controls), we found rs10994336 and rs9804190 to be nominally significantly associated with BD in this combined Nordic BD sample (N = 1,289/14,105). Nominal P was 0.015/0.018 (fixed/random effect) for rs10994336 (Bonferroni corrected P = 0.044/0.053) and 0.023 for rs9804190 (Bonferroni corrected P = 0.069). None of the SNPs were significantly associated with SZ in the combined Nordic SZ case-control sample (N = 1,724/14,410). These results further support that ANK3 is a susceptibility gene specific to BD and that more than one risk locus is involved.
PubMed ID
21972176 View in PubMed
Less detail

Association analysis of schizophrenia on 18 genes involved in neuronal migration: MDGA1 as a new susceptibility gene.

https://arctichealth.org/en/permalink/ahliterature157931
Source
Am J Med Genet B Neuropsychiatr Genet. 2008 Oct 5;147B(7):1089-100
Publication Type
Article
Date
Oct-5-2008
Author
Anna K Kähler
Srdjan Djurovic
Bettina Kulle
Erik G Jönsson
Ingrid Agartz
Håkan Hall
Stein Opjordsmoen
Klaus D Jakobsen
Thomas Hansen
Ingrid Melle
Thomas Werge
Vidar M Steen
Ole A Andreassen
Author Affiliation
TOP Project, Institute of Psychiatry, University of Oslo, Oslo, Norway. a.k.kahler@medisin.uio.no
Source
Am J Med Genet B Neuropsychiatr Genet. 2008 Oct 5;147B(7):1089-100
Date
Oct-5-2008
Language
English
Publication Type
Article
Keywords
Adult
Aged
Cell Adhesion - genetics
Cell Adhesion Molecules - genetics
Cell Movement - genetics
Female
GPI-Linked Proteins
Genetic Predisposition to Disease
Genotype
Humans
Linkage Disequilibrium
Male
Middle Aged
Nerve Tissue Proteins - metabolism
Neural Cell Adhesion Molecules
Neuroglia
Neurons - pathology
Polymorphism, Single Nucleotide
Scandinavia
Schizophrenia - genetics
Abstract
Several lines of evidence support the theory of schizophrenia (SZ) being a neurodevelopmental disorder. The structural, cytoarchitectural and functional brain abnormalities reported in patients with SZ, might be due to aberrant neuronal migration, since the final position of neurons affects neuronal function, morphology, and formation of synaptic connections. We have investigated the putative association between SZ and gene variants engaged in the neuronal migration process, by performing an association study on 839 cases and 1,473 controls of Scandinavian origin. Using a gene-wide approach, tagSNPs in 18 candidate genes have been genotyped, with gene products involved in the neuron-to-glial cell adhesion, interactions with the DISC1 protein and/or rearrangements of the cytoskeleton. Of the 289 markers tested, 19 markers located in genes MDGA1, RELN, ITGA3, DLX1, SPARCL1, and ASTN1, attained nominal significant P-values (P
PubMed ID
18384059 View in PubMed
Less detail

The association between anomalous self-experience and suicidality in first-episode schizophrenia seems mediated by depression.

https://arctichealth.org/en/permalink/ahliterature131843
Source
Compr Psychiatry. 2012 Jul;53(5):456-60
Publication Type
Article
Date
Jul-2012
Author
Elisabeth Haug
Ingrid Melle
Ole A Andreassen
Andrea Raballo
Unni Bratlien
Merete Øie
Lars Lien
Paul Møller
Author Affiliation
Division of Mental Health, Innlandet Hospital Trust, 2312 Ottestad, Norway. elisabeth.haug@sykehuset-innlandet.no
Source
Compr Psychiatry. 2012 Jul;53(5):456-60
Date
Jul-2012
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Aged
Comorbidity
Cross-Sectional Studies
Depressive Disorder - epidemiology - psychology
Early Medical Intervention
Female
Humans
Linear Models
Male
Middle Aged
Multivariate Analysis
Norway - epidemiology
Risk factors
Schizophrenia - epidemiology
Schizophrenic Psychology
Self Concept
Suicidal ideation
Suicide - prevention & control
Abstract
A recent hypothesis is that suicidality in schizophrenia may be linked to the patients' altered basic self-awareness or sense of self, termed self-disorders (SDs).
The aim of the study was to investigate whether SDs in first-episode schizophrenia spectrum disorders are related to suicidality and whether this relationship is independent of or mediated by depression or other standard clinical measures.
Self-disorders were assessed in 49 patients with first-episode schizophrenia by means of the Examination of Anomalous Self-Experience (EASE) instrument. Symptoms severity and functioning were assessed using the Structured Clinical Interview for the Positive and Negative Syndrome Scale, Calgary Depression Scale for Schizophrenia, and Global Assessment of Functioning-Split Version. Suicidality was measured by the Calgary Depression Scale for Schizophrenia item 8.
Analyses detected a significant association between current suicidality, current depression, and SDs as measured by the EASE. The effect of SDs on suicidal ideation appeared to be mediated by depression.
The interaction between anomalous self-experiences and depression could be a rational clinical target for the prevention of suicidality in the early phases of schizophrenia and supports the rationale for including assessment of SDs in early intervention efforts.
PubMed ID
21871617 View in PubMed
Less detail

Association of MCTP2 gene variants with schizophrenia in three independent samples of Scandinavian origin (SCOPE).

https://arctichealth.org/en/permalink/ahliterature152584
Source
Psychiatry Res. 2009 Aug 15;168(3):256-8
Publication Type
Article
Date
Aug-15-2009
Author
Srdjan Djurovic
Stephanie Le Hellard
Anna K Kähler
Erik G Jönsson
Ingrid Agartz
Vidar M Steen
Håkan Hall
August G Wang
Henrik B Rasmussen
Ingrid Melle
Thomas Werge
Ole A Andreassen
Author Affiliation
Institute of Psychiatry, University of Oslo, Norway. srdjan.djurovic@medisin.uio.no
Source
Psychiatry Res. 2009 Aug 15;168(3):256-8
Date
Aug-15-2009
Language
English
Publication Type
Article
Keywords
Female
Gene Frequency
Genetic Predisposition to Disease
Genome-Wide Association Study
Genotype
Humans
Male
Membrane Proteins - genetics
Polymorphism, Single Nucleotide - genetics
Scandinavia
Schizophrenia - genetics
Abstract
The MCTP2 gene is involved in intercellular signal transduction and synapse function. We genotyped 37 tagging SNPs across the MCTP2 gene to study a possible association with schizophrenia in three independent Scandinavian samples. We report, for the first time, a possible involvement of MCTP2 as a potential novel susceptibility gene for schizophrenia.
PubMed ID
19223264 View in PubMed
Less detail

Association study of PDE4B gene variants in Scandinavian schizophrenia and bipolar disorder multicenter case-control samples.

https://arctichealth.org/en/permalink/ahliterature151647
Source
Am J Med Genet B Neuropsychiatr Genet. 2010 Jan 5;153B(1):86-96
Publication Type
Article
Date
Jan-5-2010
Author
Anna K Kähler
Mona K Otnaess
Katrine V Wirgenes
Thomas Hansen
Erik G Jönsson
Ingrid Agartz
HÃ¥kan Hall
Thomas Werge
Gunnar Morken
Ole Mors
Erling Mellerup
Henrik Dam
Pernille Koefod
Ingrid Melle
Vidar M Steen
Ole A Andreassen
Srdjan Djurovic
Author Affiliation
Institute of Psychiatry, University of Oslo, Oslo, Norway. a.k.kahler@medisin.uio.no
Source
Am J Med Genet B Neuropsychiatr Genet. 2010 Jan 5;153B(1):86-96
Date
Jan-5-2010
Language
English
Publication Type
Article
Keywords
Bipolar Disorder - enzymology - genetics
Case-Control Studies
Cyclic Nucleotide Phosphodiesterases, Type 4 - genetics
Female
Haplotypes
Humans
Male
Polymorphism, Single Nucleotide
Scandinavia
Schizophrenia - enzymology - genetics
Abstract
The phosphodiesterase 4B (PDE4B), which is involved in cognitive function in animal models, is a candidate susceptibility gene for schizophrenia (SZ) and bipolar disorder (BP). Variations in PDE4B have previously been associated with SZ, with a suggested gender-specific effect. We have genotyped and analyzed 40 and 72 tagging single nucleotide polymorphisms (tagSNPs) in SZ and BP multicenter samples, respectively, from the Scandinavian Collaboration on Psychiatric Etiology (SCOPE), involving 837 SZ cases and 1,473 controls plus 594 BP cases and 1,421 partly overlapping controls. Six and 16 tagSNPs were nominally associated (0.0005
PubMed ID
19350560 View in PubMed
Less detail

Brain expressed microRNAs implicated in schizophrenia etiology.

https://arctichealth.org/en/permalink/ahliterature161432
Source
PLoS One. 2007;2(9):e873
Publication Type
Article
Date
2007
Author
Thomas Hansen
Line Olsen
Morten Lindow
Klaus D Jakobsen
Henrik Ullum
Erik Jonsson
Ole A Andreassen
Srdjan Djurovic
Ingrid Melle
Ingrid Agartz
Håkan Hall
Sally Timm
August G Wang
Thomas Werge
Author Affiliation
Research Institute of Biological Psychiatry, Sct. Hans Hospital, Roskilde, Denmark.
Source
PLoS One. 2007;2(9):e873
Date
2007
Language
English
Publication Type
Article
Keywords
Adult
Brain - metabolism
Case-Control Studies
Denmark
Female
Genotype
Humans
Male
MicroRNAs - genetics
Middle Aged
Norway
Schizophrenia - genetics
Sweden
Abstract
Protein encoding genes have long been the major targets for research in schizophrenia genetics. However, with the identification of regulatory microRNAs (miRNAs) as important in brain development and function, miRNAs genes have emerged as candidates for schizophrenia-associated genetic factors. Indeed, the growing understanding of the regulatory properties and pleiotropic effects that miRNA have on molecular and cellular mechanisms, suggests that alterations in the interactions between miRNAs and their mRNA targets may contribute to phenotypic variation.
We have studied the association between schizophrenia and genetic variants of miRNA genes associated with brain-expression using a case-control study design on three Scandinavian samples. Eighteen known SNPs within or near brain-expressed miRNAs in three samples (Danish, Swedish and Norwegian: 420/163/257 schizophrenia patients and 1006/177/293 control subjects), were analyzed. Subsequently, joint analysis of the three samples was performed on SNPs showing marginal association. Two SNPs rs17578796 and rs1700 in hsa-mir-206 (mir-206) and hsa-mit-198 (mir-198) showed nominal significant allelic association to schizophrenia in the Danish and Norwegian sample respectively (P = 0.0021 & p = 0.038), of which only rs17578796 was significant in the joint sample. In-silico analysis revealed that 8 of the 15 genes predicted to be regulated by both mir-206 and mir-198, are transcriptional targets or interaction partners of the JUN, ATF2 and TAF1 connected in a tight network. JUN and two of the miRNA targets (CCND2 and PTPN1) in the network have previously been associated with schizophrenia.
We found nominal association between brain-expressed miRNAs and schizophrenia for rs17578796 and rs1700 located in mir-206 and mir-198 respectively. These two miRNAs have a surprising large number (15) of targets in common, eight of which are also connected by the same transcription factors.
Notes
Cites: Schizophr Res. 1999 Nov 9;40(1):23-910541003
Cites: Arch Gen Psychiatry. 2000 Jan;57(1):65-7310632234
Cites: Am J Med Genet. 2001 Dec 8;105(8):794-80011803533
Cites: Science. 2002 May 3;296(5569):916-911988577
Cites: Genet Epidemiol. 2003 Sep;25(2):115-2112916020
Cites: Genetics. 2003 Aug;164(4):1567-8712930761
Cites: Genome Res. 2003 Nov;13(11):2498-50414597658
Cites: Nature. 2003 Dec 18;426(6968):845-914685240
Cites: Proc Natl Acad Sci U S A. 2004 Jan 6;101(1):360-514691248
Cites: Genome Biol. 2004;5(3):R1315003116
Cites: Psychopharmacology (Berl). 2004 Jun;174(1):151-6215205886
Cites: Mol Psychiatry. 2004 Jul;9(7):684-97, 64315098003
Cites: Nature. 2004 Aug 12;430(7001):785-915306811
Cites: J Neurosci Res. 2004 Sep 15;77(6):858-6615334603
Cites: Cold Spring Harb Symp Quant Biol. 2003;68:69-7815338605
Cites: Brain. 1999 Apr;122 ( Pt 4):593-62410219775
Cites: PLoS Biol. 2004 Nov;2(11):e36315502875
Cites: Cell. 2005 Jan 14;120(1):15-2015652477
Cites: Science. 2005 May 20;308(5725):1149-5415790807
Cites: Eur J Hum Genet. 2005 Aug;13(8):894-715970949
Cites: J Neurochem. 2005 Aug;94(4):896-90516092937
Cites: Nord J Psychiatry. 2005;59(3):209-1216195122
Cites: Proc Natl Acad Sci U S A. 2005 Nov 8;102(45):16426-3116260724
Cites: Nord J Psychiatry. 2005;59(6):457-6416316898
Cites: Science. 2005 Dec 16;310(5755):1817-2116308420
Cites: Biochemistry (Mosc). 2005 Dec;70(12):1404-716417465
Cites: Proc Natl Acad Sci U S A. 2006 Feb 14;103(7):2422-716461918
Cites: Genes Dev. 2006 Mar 1;20(5):515-2416510870
Cites: Stem Cells. 2006 Apr;24(4):857-6416357340
Cites: Prog Neuropsychopharmacol Biol Psychiatry. 2006 Jul;30(5):924-3316581172
Cites: J Physiol. 2006 Sep 1;575(Pt 2):333-4116809366
Cites: Psychopathology. 2006;39(6):269-7616960465
Cites: Psychopathology. 2006;39(6):286-9516960467
Cites: Am J Hum Genet. 2007 Mar;80(3):393-40617273961
Cites: Genome Biol. 2007;8(2):R2717326821
Cites: Nature. 2007 Jun 7;447(7145):661-7817554300
Cites: Am J Hum Genet. 2007 Sep;81(3):559-7517701901
Cites: Nature. 2006 Jan 19;439(7074):283-916421561
Cites: Prog Brain Res. 2005;147:319-4515581715
Cites: Mol Psychiatry. 2005 Jan;10(1):27-3915340352
Cites: Mol Psychiatry. 2005 Jan;10(1):69-7815381925
Cites: Bioinformatics. 2005 Jan 15;21(2):263-515297300
PubMed ID
17849003 View in PubMed
Less detail

Cannabis use and premorbid functioning as predictors of poorer neurocognition in schizophrenia spectrum disorder.

https://arctichealth.org/en/permalink/ahliterature118693
Source
Schizophr Res. 2013 Jan;143(1):84-9
Publication Type
Article
Date
Jan-2013
Author
P Andreas Ringen
Ingrid Melle
Akiah O Berg
Ingrid Agartz
Olav Spigset
Carmen Simonsen
Kjetil Sundet
Ole A Andreassen
Author Affiliation
KG Jebsen Centre for Psychosis Research, Division of Mental Health and Addiction, Oslo University Hospital, N-0424 Oslo, Norway. p.a.ringen@medisin.uio.no
Source
Schizophr Res. 2013 Jan;143(1):84-9
Date
Jan-2013
Language
English
Publication Type
Article
Keywords
Adaptation, Psychological
Adult
Attention
Cannabinoids - urine
Cognition Disorders - diagnosis - etiology
Executive Function
Female
Humans
Male
Marijuana Abuse - complications - epidemiology - psychology - urine
Memory
Neuropsychological Tests
Norway
Predictive value of tests
Psychiatric Status Rating Scales
Psychomotor Performance
Regression Analysis
Schizophrenia - complications - epidemiology
Schizophrenic Psychology
Verbal Learning
Young Adult
Abstract
Evidence of associations between neurocognitive function and cannabis use in schizophrenia is inconclusive. However, direct measures of cannabis intake and premorbid function are rarely explored in this context. We investigated the relation between cannabis use, determined by its presence in urine, and neurocognitive functioning in schizophrenia controlling for the potential bias of premorbid functioning.
Naturalistic study of 364 patients with schizophrenia spectrum disorder from catchment areas in Oslo, Norway. Hierarchical multiple regression analyses were used to assess the relationship between cannabis in urine and measures of neurocognitive functioning, with adjustment for confounders, including premorbid functioning.
Cannabis was detected in the urine of 21 patients, who had significant dysfunction in several neurocognitive domains independent of a current diagnosis of cannabis abuse. However, level of premorbid functioning explained the associations for all measures.
Differences in premorbid functioning may explain apparent differences in neurocognitive function between schizophrenia spectrum patients using cannabis or not. The findings suggest that illness-related traits present early in life can affect both later cannabis use and neurocognition, probably by complex mechanisms.
PubMed ID
23178107 View in PubMed
Less detail

Cannabis use is associated with 3years earlier onset of schizophrenia spectrum disorder in a naturalistic, multi-site sample (N=1119).

https://arctichealth.org/en/permalink/ahliterature277445
Source
Schizophr Res. 2016 Jan;170(1):217-21
Publication Type
Article
Date
Jan-2016
Author
Siri Helle
Petter Andreas Ringen
Ingrid Melle
Tor-Ketil Larsen
Rolf Gjestad
Erik Johnsen
Trine Vik Lagerberg
Ole A Andreassen
Rune Andreas Kroken
Inge Joa
Wenche Ten Velden Hegelstad
Else-Marie Løberg
Source
Schizophr Res. 2016 Jan;170(1):217-21
Date
Jan-2016
Language
English
Publication Type
Article
Keywords
Adult
Age of Onset
Cannabis
Family
Female
Humans
Male
Marijuana Abuse - complications - epidemiology
Norway - epidemiology
Psychotic Disorders - complications - epidemiology
Regression Analysis
Schizophrenia - complications - epidemiology
Sex Factors
Young Adult
Abstract
Patients with schizophrenia spectrum disorders and substance use may have an earlier onset of illness compared to those without substance use. Most previous studies have, however, too small samples to control for confounding variables and the effect of specific types of substances. The present study aimed to examine the relationship between substance use and age at onset, in addition to the influence of possible confounders and specific substances, in a large and heterogeneous multisite sample of patients with schizophrenia spectrum disorders.
The patients (N=1119) were recruited from catchment areas in Oslo, Stavanger and Bergen, Norway, diagnosed according to DSM-IV and screened for substance use history. Linear regression analysis was used to examine the relationship between substance use and age at onset of illness.
Patients with substance use (n=627) had about 3years earlier age at onset (23.0years; SD 7.1) than the abstinent group (n=492; 25.9years; SD 9.7). Only cannabis use was statistically significantly related to earlier age at onset. Gender or family history of psychosis did not influence the results.
Cannabis use is associated with 3years earlier onset of psychosis.
PubMed ID
26682958 View in PubMed
Less detail

Catechol O-methyltransferase variants and cognitive performance in schizophrenia and bipolar disorder versus controls.

https://arctichealth.org/en/permalink/ahliterature142371
Source
Schizophr Res. 2010 Sep;122(1-3):31-7
Publication Type
Article
Date
Sep-2010
Author
Katrine V Wirgenes
Srdjan Djurovic
Kjetil Sundet
Ingrid Agartz
Morten Mattingsdal
Lavinia Athanasiu
Ingrid Melle
Ole A Andreassen
Author Affiliation
Institute of Psychiatry, University of Oslo, Oslo, Norway.
Source
Schizophr Res. 2010 Sep;122(1-3):31-7
Date
Sep-2010
Language
English
Publication Type
Article
Keywords
Adult
Analysis of Variance
Bipolar Disorder - complications - genetics
Catechol O-Methyltransferase - genetics
Cognition Disorders - etiology - genetics
Female
Gene Frequency - genetics
Genotype
Humans
Male
Methionine - genetics
Neuropsychological Tests
Norway - epidemiology
Polymorphism, Single Nucleotide - genetics
Schizophrenia - complications - genetics
Valine - genetics
Abstract
The gene encoding Catechol O-methyltransferase (COMT), a dopamine catabolic enzyme, is an important candidate gene in several psychiatric disorders. Several studies have shown an association between the functional Val(158)Met polymorphism and cognitive performance. However, the results have been inconsistent and there are few studies addressing other COMT single nucleotide polymorphisms (SNPs).
We investigated SNPs across the whole COMT gene, including the Val(158)Met polymorphism, for a putative effect on working memory, executive function and IQ in 315 patients with schizophrenia or bipolar disorder and 340 healthy controls.
We replicated the association between the Val(158)Met variant and working memory performance, and found a significant interaction between this SNP and diagnosis, with patients with schizophrenia showing a specific, reduced performance on the 2-back test. Several other COMT SNPs were associated with different cognitive functions, but did not remain significant after controlling for multiple testing. We also found significant interaction effects between the SNP variants and gender.
The present study replicates earlier findings showing an association between the functional Val(158)Met polymorphism and working memory performance, with schizophrenia subjects particularly vulnerable. Furthermore, our findings suggest that other parts of the COMT gene seem to affect several related cognitive domains, which further support the notion that COMT is a modifier gene in prefrontal dopamine functioning.
PubMed ID
20605701 View in PubMed
Less detail

45 records – page 1 of 5.