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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
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Childhood trauma is associated with severe clinical characteristics of bipolar disorders.

https://arctichealth.org/en/permalink/ahliterature106157
Source
J Clin Psychiatry. 2013 Oct;74(10):991-8
Publication Type
Article
Date
Oct-2013
Author
Bruno Etain
Monica Aas
Ole A Andreassen
Steinar Lorentzen
Ingrid Dieset
Sebastien Gard
Jean-Pierre Kahn
Frank Bellivier
Marion Leboyer
Ingrid Melle
Chantal Henry
Author Affiliation
Pôle de Psychiatrie, Hôpital Henri Mondor-Albert Chenevier, Assistance Publique Hôpitaux de Paris (APHP); and Institut National de la Santé et de la Recherche Médicale (INSERM) U955.
Source
J Clin Psychiatry. 2013 Oct;74(10):991-8
Date
Oct-2013
Language
English
Publication Type
Article
Keywords
Adult
Adult Survivors of Child Abuse - psychology - statistics & numerical data
Age of Onset
Bipolar Disorder - diagnosis - epidemiology - etiology - psychology
Child
Child Abuse - classification - diagnosis - psychology - statistics & numerical data
Diagnostic and Statistical Manual of Mental Disorders
Female
France - epidemiology
Humans
Male
Middle Aged
Norway - epidemiology
Psychiatric Status Rating Scales
Questionnaires
Statistics as Topic
Suicide, Attempted - psychology - statistics & numerical data
Abstract
Beyond genetic risk variants, the pathophysiology of bipolar disorders is likely to be partly determined by environmental susceptibility factors. Our study is one of the first to investigate, in a large sample of well-characterized bipolar patients, associations between clinical presentations and childhood trauma subtypes, including neglect and abuse items.
587 patients with DSM-IV-defined bipolar disorder were recruited from France and Norway between 1996-2008 and 2007-2012, respectively. History of childhood trauma was obtained using the Childhood Trauma Questionnaire. Clinical variables were assessed with the Structured Clinical Interview for DSM-IV Axis I Disorders (Norwegian sample) or the Diagnostic Interview for Genetic Studies (French sample).
Earlier age at onset of bipolar illness, suicide attempts, rapid cycling, and an increased number of depressive episodes each had significant associations (P = .001) with at least 1 subtype of childhood trauma (emotional abuse, sexual abuse, and emotional neglect). Multivariate analyses investigating trauma variables together showed that both emotional and sexual abuse were independent predictors of lower age at onset (P = .002 for each) and history of suicide attempts (OR = 1.60 [95% CI, 1.07 to 2.39], P = .023; OR = 1.80 [95% CI, 1.14 to 2.86], P = .012, respectively), while sexual abuse was the strongest predictor of rapid cycling (OR = 2.04 [95% CI, 1.21 to 3.42], P = .007). Females reported overall higher childhood trauma frequency and greater associations to clinical expressions than males (P values
PubMed ID
24229750 View in PubMed
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Expression and genetic variability of PCDH11Y, a gene specific to Homo sapiens and candidate for susceptibility to psychiatric disorders.

https://arctichealth.org/en/permalink/ahliterature171675
Source
Am J Med Genet B Neuropsychiatr Genet. 2006 Jan 5;141B(1):67-70
Publication Type
Article
Date
Jan-5-2006
Author
Christelle M Durand
Caroline Kappeler
Catalina Betancur
Richard Delorme
Hélène Quach
Hany Goubran-Botros
Jonas Melke
Gudrun Nygren
Nadia Chabane
Franck Bellivier
Andrei Szoke
Franck Schurhoff
Maria Rastam
Henrik Anckarsäter
Christopher Gillberg
Marion Leboyer
Thomas Bourgeron
Author Affiliation
Human Genetics and Cognitive Functions, Institut Pasteur, 25 rue du Docteur Roux, 75724 Paris Cedex 15, France.
Source
Am J Med Genet B Neuropsychiatr Genet. 2006 Jan 5;141B(1):67-70
Date
Jan-5-2006
Language
English
Publication Type
Article
Keywords
Amino Acid Sequence
Attention Deficit Disorder with Hyperactivity - genetics
Autistic Disorder - genetics
Bipolar Disorder - genetics
Brain - metabolism
Cadherins - genetics
DNA Mutational Analysis
France
Gene Expression
Gene Frequency
Genetic Predisposition to Disease - genetics
Haplotypes
Humans
Male
Mental Disorders - genetics
Molecular Sequence Data
Mutation
Mutation, Missense
Polymorphism, Genetic
RNA - genetics - metabolism
Reverse Transcriptase Polymerase Chain Reaction
Sequence Homology, Amino Acid
Sweden
Abstract
Synaptogenesis, the formation of functional synapses, is a crucial step for the development of the central nervous system. Among the genes involved in this process are cell adhesion molecules, such as protocadherins and neuroligins, which are essential factors for the identification of the appropriate partner cell and the formation of synapses. In this work, we studied the expression and the genetic variability of two closely related members of the protocadherin family PCDH11X/Y, located on the X and the Y chromosome, respectively. PCDH11Y is one of the rare genes specific to the hominoid lineage, being absent in other primates. Expression analysis indicated that transcripts of the PCDH11X/Y genes are mainly detected in the cortex of the human brain. Mutation screening of 30 individuals with autism identified two PCDH11Y polymorphic amino acid changes, F885V and K980N. These variations are in complete association, appeared during human evolution approximately 40,000 years ago and represent informative polymorphisms to study Y chromosome variability in populations. We studied the frequency of these variants in males with autism spectrum disorders (n = 110), attention deficit hyperactivity disorder (ADHD; n = 61), bipolar disorder (n = 61), obsessive-compulsive disorder (n = 51), or schizophrenia (n = 61) and observed no significant differences when compared to ethnically-matched control populations. These findings do not support the role of PCDH11Y, or more generally of a frequent specific Y chromosome, in the susceptibility to these neuropsychiatric disorders.
PubMed ID
16331680 View in PubMed
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Investigation of two variants in the DOPA decarboxylase gene in patients with autism.

https://arctichealth.org/en/permalink/ahliterature31592
Source
Am J Med Genet. 2002 May 8;114(4):466-70
Publication Type
Article
Date
May-8-2002
Author
Marlene B Lauritsen
Anders D Børglum
Catalina Betancur
Anne Philippe
Torben A Kruse
Marion Leboyer
Henrik Ewald
Author Affiliation
Department of Psychiatric Demography, Institute for Basic Psychiatric Research, Psychiatric Hospital in Aarhus, Risskov, Denmark.
Source
Am J Med Genet. 2002 May 8;114(4):466-70
Date
May-8-2002
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Autistic Disorder - genetics
Child
Child, Preschool
Dopa Decarboxylase - genetics
Female
Genotype
Haplotypes
Humans
Male
Research Support, Non-U.S. Gov't
Sequence Deletion
Abstract
Though genetic risk factors are important for the development of autism, no specific risk alleles have yet been identified. DOPA decarboxylase (DDC) is involved in both the catecholaminergic and serotonergic pathways and may be considered a functional candidate gene for autism. The present study is the first to test if two new variants of possible functional significance in the DDC gene increase the susceptibility to autism. A total of 90 parent-offspring trios recruited in Denmark and France were investigated using the transmission disequilibrium test (TDT). We found no evidence of linkage disequilibrium between autism and either of the two polymorphisms. Nor did we find linkage disequilibrium between autism and haplotypes of the two variants using a multiallelic TDT. These findings suggest that the DDC gene is unlikely to play a major role in the development of autism in our data set.
PubMed ID
11992572 View in PubMed
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National funding for mental health research in Finland, France, Spain and the United Kingdom.

https://arctichealth.org/en/permalink/ahliterature291605
Source
Eur Neuropsychopharmacol. 2017 09; 27(9):892-899
Publication Type
Comparative Study
Journal Article
Date
09-2017
Author
Jean-Baptiste Hazo
Coralie Gandré
Marion Leboyer
Carla Obradors-Tarragó
Stefano Belli
David McDaid
A-La Park
Maria Victoria Maliandi
Kristian Wahlbeck
Til Wykes
Jim van Os
Josep Maria Haro
Karine Chevreul
Author Affiliation
ECEVE, UMRS 1123, Université Paris Diderot, Sorbonne Paris Cité, INSERM, Paris, France; AP-HP, URC-Eco, DHU Pepsy, F-75004 Paris, France; Foundation FondaMental, French National Science Foundation, Créteil, France. Electronic address: jeanbaptiste.hazo@urc-eco.fr.
Source
Eur Neuropsychopharmacol. 2017 09; 27(9):892-899
Date
09-2017
Language
English
Publication Type
Comparative Study
Journal Article
Keywords
Biomedical Research - economics
Charities - economics
Finland
France
Humans
Mental Health - economics
Spain
United Kingdom
Abstract
As part of the Roamer project, we aimed at revealing the share of health research budgets dedicated to mental health, as well as on the amounts allocated to such research for four European countries. Finland, France, Spain and the United Kingdom national public and non-profit funding allocated to mental health research in 2011 were investigated using, when possible, bottom-up approaches. Specifics of the data collection varied from country to country. The total amount of public and private not for profit mental health research funding for Finland, France, Spain and the UK was €10·2, €84·8, €16·8, and €127·6 million, respectively. Charities accounted for a quarter of the funding in the UK and less than six per cent elsewhere. The share of health research dedicated to mental health ranged from 4·0% in the UK to 9·7% in Finland. When compared to the DALY attributable to mental disorders, Spain, France, Finland, and the UK invested respectively €12·5, €31·2, €39·5, and €48·7 per DALY. Among these European countries, there is an important gap between the level of mental health research funding and the economic and epidemiologic burden of mental disorders.
PubMed ID
28647453 View in PubMed
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No Human Tryptophan Hydroxylase-2 Gene R441H Mutation in a Large Cohort of Psychiatric Patients and Control Subjects.

https://arctichealth.org/en/permalink/ahliterature45588
Source
Biol Psychiatry. 2006 Mar 31;
Publication Type
Article
Date
Mar-31-2006
Author
Richard Delorme
Christelle M Durand
Catalina Betancur
Michael Wagner
Stephan Ruhrmann
Hans-Juergen Grabe
Gudrun Nygren
Christopher Gillberg
Marion Leboyer
Thomas Bourgeron
Philippe Courtet
Fabrice Jollant
Catherine Buresi
Jean-Michel Aubry
Patrick Baud
Guido Bondolfi
Gilles Bertschy
Nader Perroud
Alain Malafosse
Author Affiliation
Human Genetics and Cognitive Functions (RD, CMD, TB, ML), Pasteur Institute, Paris, France; INSERM U513 (RD, CBe, ML), Université Paris XII, Créteil, France.
Source
Biol Psychiatry. 2006 Mar 31;
Date
Mar-31-2006
Language
English
Publication Type
Article
Abstract
BACKGROUND: It was recently reported that a rare functional variant, R441H, in the human tryptophan hydroxylase-2 gene (hTPH2) could represent an important risk factor for unipolar major depression (UP) since it was originally found in 10% of UP patients (vs. 1.4% in control subjects). METHODS: We explored the occurrence of this variation in patients with affective disorders (n = 646), autism spectrum disorders (n = 224), and obsessive-compulsive disorder (OCD) (n = 201); in healthy volunteers with no psychiatric disorders (n = 246); and in an ethnic panel of control individuals from North Africa, Sub-Saharan Africa, India, China, and Sweden (n = 277). RESULTS: Surprisingly, we did not observe the R441H variant in any of the individuals screened (3188 independent chromosomes). CONCLUSIONS: Our results do not confirm the role of the R441H mutation of the hTPH2 gene in the susceptibility to UP. The absence of the variant from a large cohort of psychiatric patients and control subjects suggests that the findings reported in the original study could be due to a genotyping error or to stratification of the initial population reported. Additional data by other groups should contribute to the clarification of the discrepancy between our results and those previous published.
PubMed ID
16581035 View in PubMed
Less detail

Psychometric properties of the Affective Lability Scale (54 and 18-item version) in patients with bipolar disorder, first-degree relatives, and healthy controls.

https://arctichealth.org/en/permalink/ahliterature277357
Source
J Affect Disord. 2015 Feb 1;172:375-80
Publication Type
Article
Date
Feb-1-2015
Author
Monica Aas
Geir Pedersen
Chantal Henry
Thomas Bjella
Frank Bellivier
Marion Leboyer
Jean-Pierre Kahn
Renaud F Cohen
Sebastien Gard
Sofie R Aminoff
Trine V Lagerberg
Ole A Andreassen
Ingrid Melle
Bruno Etain
Source
J Affect Disord. 2015 Feb 1;172:375-80
Date
Feb-1-2015
Language
English
Publication Type
Article
Keywords
Adult
Affect
Bipolar Disorder - psychology
Case-Control Studies
Factor Analysis, Statistical
Family
Female
France
Humans
Male
Norway
Psychiatric Status Rating Scales
Psychometrics
Reproducibility of Results
Abstract
The aim of this study was to investigate the psychometric properties of the original 54 item version (ALS-54) and the short 18 item version (ALS-18) of the Affective Lability Scale (ALS) in patients with bipolar disorders, their first-degree relatives and healthy controls. Internal Consistency and Confirmatory Factor Analysis were performed, comparing clinical and non-clinical group comparisons on ALS scores.
A total of 993 participants (patients with bipolar disorders [n=422], first-degree relatives [n=201] and controls [n=370]) were recruited from France and Norway. Diagnosis and clinical characteristics were assessed using the Structured Clinical Interview for DSM-IV Axis I disorders (SCID-I), or the Diagnostic Interview for Genetic Studies (DIGS). Affective lability was measured using the ALS-54 and ALS-18.
Both ALS-54 and ALS-18 showed high internal consistency, but the subdimensions of both versions were highly inter-correlated. From confirmatory factor analysis both versions revealed acceptable to good model fit. Patients had significantly higher ALS scores compared to controls, with affected first-degree relatives presenting intermediate scores.
Both the original ALS-54 version and the short ALS-18 version showed good psychometric properties. They also discriminated between patients with a bipolar disorder (high ALS), first degree relatives (intermediate ALS), and healthy controls (low ALS). A high correlation between ALS items for both versions was observed. Our study supports reducing the scale from 54 to 18 items.
PubMed ID
25451440 View in PubMed
Less detail

SHANK1 Deletions in Males with Autism Spectrum Disorder.

https://arctichealth.org/en/permalink/ahliterature125229
Source
Am J Hum Genet. 2012 May 4;90(5):879-87
Publication Type
Article
Date
May-4-2012
Author
Daisuke Sato
Anath C Lionel
Claire S Leblond
Aparna Prasad
Dalila Pinto
Susan Walker
Irene O'Connor
Carolyn Russell
Irene E Drmic
Fadi F Hamdan
Jacques L Michaud
Volker Endris
Ralph Roeth
Richard Delorme
Guillaume Huguet
Marion Leboyer
Maria Rastam
Christopher Gillberg
Mark Lathrop
Dimitri J Stavropoulos
Evdokia Anagnostou
Rosanna Weksberg
Eric Fombonne
Lonnie Zwaigenbaum
Bridget A Fernandez
Wendy Roberts
Gudrun A Rappold
Christian R Marshall
Thomas Bourgeron
Peter Szatmari
Stephen W Scherer
Author Affiliation
The Centre for Applied Genomics and Program in Genetics and Genome Biology, The Hospital for Sick Children, Toronto, Ontario, Canada.
Source
Am J Hum Genet. 2012 May 4;90(5):879-87
Date
May-4-2012
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Canada
Child
Child Development Disorders, Pervasive - genetics - physiopathology
Child, Preschool
DNA Copy Number Variations
Europe
Female
Humans
Intellectual Disability - genetics - physiopathology
Male
Mutation
Nerve Tissue Proteins - genetics - metabolism
Neurons - metabolism
Pedigree
Sequence Deletion
Synapses - genetics - metabolism
Abstract
Recent studies have highlighted the involvement of rare (15,000 controls (p = 0.009). The discovery of apparent reduced penetrance of ASD in females bearing inherited autosomal SHANK1 deletions provides a possible contributory model for the male gender bias in autism. The data are also informative for clinical-genetics interpretations of both inherited and sporadic forms of ASD involving SHANK1.
Notes
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PubMed ID
22503632 View in PubMed
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8 records – page 1 of 1.