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Article ; Online: The dynamic interplay between sleep and mood: an intensive longitudinal study of individuals with bipolar disorder.

Lewis, K J S / Tilling, K / Gordon-Smith, K / Saunders, K E A / Di Florio, A / Jones, L / Jones, I / O'Donovan, M C / Heron, J

Psychological medicine

2022 Volume 53, Issue 8, Page(s) 3345–3354

Abstract: Background: Sleep disturbances are important symptoms to monitor in people with bipolar disorder (BD) but the precise longitudinal relationships between sleep and mood remain unclear. We aimed to examine associations between stable and dynamic aspects ... ...

Abstract	Background: Sleep disturbances are important symptoms to monitor in people with bipolar disorder (BD) but the precise longitudinal relationships between sleep and mood remain unclear. We aimed to examine associations between stable and dynamic aspects of sleep and mood in people with BD, and assess individual differences in the strength of these associations. Methods: Participants ( Results: Increased variability in insomnia symptoms was associated with increased mood variability. In the sample as a whole, we found strong evidence of bidirectional relationships between insomnia and depressive symptoms but only weak support for bidirectional relationships between insomnia and (hypo)manic symptoms. We found substantial variability between participants in the strength of prospective associations between insomnia and mood, which depended on age, gender, bipolar subtype, and a history of rapid cycling. Conclusions: Our results highlight the importance of monitoring sleep in people with BD. However, researchers and clinicians investigating the association between sleep and mood should consider subgroup differences in this relationship. Advances in digital technology mean that intensive longitudinal data on sleep and mood are becoming increasingly available. Novel methods to analyse these data present an exciting opportunity for furthering our understanding of BD.
MeSH term(s)	Humans ; Bipolar Disorder/complications ; Longitudinal Studies ; Sleep Initiation and Maintenance Disorders/epidemiology ; Sleep Initiation and Maintenance Disorders/complications ; Affect ; Sleep
Language	English
Publishing date	2022-01-25
Publishing country	England
Document type	Journal Article
ZDB-ID	217420-0
ISSN	1469-8978 ; 0033-2917
ISSN (online)	1469-8978
ISSN	0033-2917
DOI	10.1017/S0033291721005377
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Article ; Online: Genetic risk for schizophrenia is associated with altered visually-induced gamma band activity: evidence from a population sample stratified polygenic risk.

Dimitriadis, S I / Perry, G / Foley, S F / Tansey, K E / Jones, D K / Holmans, P / Zammit, S / Hall, J / O'Donovan, M C / Owen, M J / Singh, K D / Linden, D E

Translational psychiatry

2021 Volume 11, Issue 1, Page(s) 592

Abstract: Gamma oscillations (30-90 Hz) have been proposed as a signature of cortical visual information processing, particularly the balance between excitation and inhibition, and as a biomarker of neuropsychiatric diseases. Magnetoencephalography (MEG) provides ... ...

Abstract	Gamma oscillations (30-90 Hz) have been proposed as a signature of cortical visual information processing, particularly the balance between excitation and inhibition, and as a biomarker of neuropsychiatric diseases. Magnetoencephalography (MEG) provides highly reliable visual-induced gamma oscillation estimates, both at sensor and source level. Recent studies have reported a deficit of visual gamma activity in schizophrenia patients, in medication naive subjects, and high-risk clinical participants, but the genetic contribution to such a deficit has remained unresolved. Here, for the first time, we use a genetic risk score approach to assess the relationship between genetic risk for schizophrenia and visual gamma activity in a population-based sample drawn from a birth cohort. We compared visual gamma activity in a group (N = 104) with a high genetic risk profile score for schizophrenia (SCZ-PRS) to a group with low SCZ-PRS (N = 99). Source-reconstructed V1 activity was extracted using beamformer analysis applied to MEG recordings using individual MRI scans. No group differences were found in the induced gamma peak amplitude or peak frequency. However, a non-parametric statistical contrast of the response spectrum revealed more robust group differences in the amplitude of high-beta/gamma power across the frequency range, suggesting that overall spectral shape carries important biological information beyond the individual frequency peak. Our findings show that changes in gamma band activity correlate with liability to schizophrenia and suggest that the index changes to synaptic function and neuronal firing patterns that are of pathophysiological relevance rather than consequences of the disorder.
MeSH term(s)	Birth Cohort ; Gamma Rhythm ; Humans ; Magnetoencephalography ; Risk Factors ; Schizophrenia/genetics
Language	English
Publishing date	2021-11-16
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2609311-X
ISSN	2158-3188 ; 2158-3188
ISSN (online)	2158-3188
ISSN	2158-3188
DOI	10.1038/s41398-021-01678-z
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Article ; Online: Genetic risk for schizophrenia is associated with increased proportion of indirect connections in brain networks revealed by a semi-metric analysis: evidence from population sample stratified for polygenic risk.

Dimitriadis, S I / Perry, G / Lancaster, T M / Tansey, K E / Singh, K D / Holmans, P / Pocklington, A / Davey Smith, G / Zammit, S / Hall, J / O'Donovan, M C / Owen, M J / Jones, D K / Linden, D E

Cerebral cortex (New York, N.Y. : 1991)

2022 Volume 33, Issue 6, Page(s) 2997–3011

Abstract: Research studies based on tractography have revealed a prominent reduction of asymmetry in some key white-matter tracts in schizophrenia (SCZ). However, we know little about the influence of common genetic risk factors for SCZ on the efficiency of ... ...

Abstract	Research studies based on tractography have revealed a prominent reduction of asymmetry in some key white-matter tracts in schizophrenia (SCZ). However, we know little about the influence of common genetic risk factors for SCZ on the efficiency of routing on structural brain networks (SBNs). Here, we use a novel recall-by-genotype approach, where we sample young adults from a population-based cohort (ALSPAC:N genotyped = 8,365) based on their burden of common SCZ risk alleles as defined by polygenic risk score (PRS). We compared 181 individuals at extremes of low (N = 91) or high (N = 90) SCZ-PRS under a robust diffusion MRI-based graph theoretical SBN framework. We applied a semi-metric analysis revealing higher SMR values for the high SCZ-PRS group compared with the low SCZ-PRS group in the left hemisphere. Furthermore, a hemispheric asymmetry index showed a higher leftward preponderance of indirect connections for the high SCZ-PRS group compared with the low SCZ-PRS group (PFDR < 0.05). These findings might indicate less efficient structural connectivity in the higher genetic risk group. This is the first study in a population-based sample that reveals differences in the efficiency of SBNs associated with common genetic risk variants for SCZ.
MeSH term(s)	Young Adult ; Humans ; Schizophrenia/diagnostic imaging ; Schizophrenia/genetics ; Genetic Predisposition to Disease/genetics ; Brain/diagnostic imaging ; Risk Factors ; Genotype
Language	English
Publishing date	2022-07-08
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1077450-6
ISSN	1460-2199 ; 1047-3211
ISSN (online)	1460-2199
ISSN	1047-3211
DOI	10.1093/cercor/bhac256
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Article ; Online: The relative contribution of common and rare genetic variants to ADHD.

Martin, J / O'Donovan, M C / Thapar, A / Langley, K / Williams, N

Translational psychiatry

2015 Volume 5, Page(s) e506

Abstract: Attention deficit hyperactivity disorder (ADHD) is highly heritable. Genome-wide molecular studies show an increased burden of large, rare copy-number variants (CNVs) in children with ADHD compared with controls. Recent polygenic risk score analyses have ...

Abstract	Attention deficit hyperactivity disorder (ADHD) is highly heritable. Genome-wide molecular studies show an increased burden of large, rare copy-number variants (CNVs) in children with ADHD compared with controls. Recent polygenic risk score analyses have also shown that en masse common variants are enriched in ADHD cases compared with population controls. The relationship between these common and rare variants has yet to be explored. In this study, we tested whether children with ADHD with (N=60) a large (>500 kb), rare (<1% frequency) CNV differ by polygenic risk scores for ADHD to children with ADHD without such CNVs (N=421). We also compared ADHD polygenic scores in ADHD children with and without CNVs with a group of population controls (N=4670; of whom N=397 had CNVs). The results show that children with ADHD with large, rare CNVs have lower polygenic scores than children without such CNVs (odds ratio (OR)=0.73, P=0.023). Although ADHD children without CNVs had higher scores than controls (OR=1.18, P=0.0031), this difference was not observed for ADHD children with CNVs (OR=0.86, P=0.27). These results are consistent with a polygenic liability threshold model of ADHD with both common and rare variants involved.
MeSH term(s)	Adolescent ; Attention Deficit Disorder with Hyperactivity/genetics ; Case-Control Studies ; Child ; DNA Copy Number Variations ; Female ; Genetic Predisposition to Disease ; Humans ; Male ; Multifactorial Inheritance/genetics ; Polymorphism, Single Nucleotide
Language	English
Publishing date	2015-02-10
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2609311-X
ISSN	2158-3188 ; 2158-3188
ISSN (online)	2158-3188
ISSN	2158-3188
DOI	10.1038/tp.2015.5
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Article ; Online: Recent genomic advances in schizophrenia.

Doherty, J L / O'Donovan, M C / Owen, M J

Clinical genetics

2012 Volume 81, Issue 2, Page(s) 103–109

Abstract: Recent studies have supported the hypothesis based upon expectations from population genetics that the high heritability of schizophrenia reflects a combination of relatively common alleles of small effect and rare alleles some with relatively large ... ...

Abstract	Recent studies have supported the hypothesis based upon expectations from population genetics that the high heritability of schizophrenia reflects a combination of relatively common alleles of small effect and rare alleles some with relatively large effects. Genome-wide association studies have identified a number of risk loci at genome-wide levels of significance as well as evidence for a substantial burden of common risk loci. Moreover these recent findings suggest genetic overlap with bipolar disorder which has traditionally been assumed to be genetically distinct from schizophrenia. Genome-wide studies of at least one class of relatively uncommon variant, submicroscopic chromosomal abnormalities often referred to as copy number variations (CNVs), suggest that these confer high risk of schizophrenia. There is evidence both for an increased burden of large, rare CNVs in schizophrenia and that risk is conferred by a number of specific large CNVs as well as by deletions of NRXN1 which encodes the synaptic scaffolding protein neurexin 1. Many of these CNVs have been implicated in autism, mental retardation, epilepsy and other neurodevelopment disorders. These findings have implications for pathogenesis and nosology of schizophrenia and related disorders, and for future genetic studies.
MeSH term(s)	DNA Copy Number Variations ; Genetic Predisposition to Disease ; Genome-Wide Association Study ; Genomics ; Humans ; Polymorphism, Single Nucleotide ; Schizophrenia/diagnosis ; Schizophrenia/epidemiology ; Schizophrenia/genetics
Language	English
Publishing date	2012-02
Publishing country	Denmark
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	221209-2
ISSN	1399-0004 ; 0009-9163
ISSN (online)	1399-0004
ISSN	0009-9163
DOI	10.1111/j.1399-0004.2011.01773.x
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Article: Strong evidence for multiple psychosis susceptibility genes - a rejoinder to Crow.

O'Donovan, M C / Craddock, N / Owen, M J

Psychological medicine

2009 Volume 39, Issue 1, Page(s) 170–171

MeSH term(s)	Bipolar Disorder/genetics ; Bipolar Disorder/psychology ; Genetic Predisposition to Disease/genetics ; Genetic Predisposition to Disease/psychology ; Humans ; Psychotic Disorders/genetics ; Psychotic Disorders/psychology ; Schizophrenia/genetics ; Schizophrenic Psychology
Language	English
Publishing date	2009-01
Publishing country	England
Document type	Comment ; Letter
ZDB-ID	217420-0
ISSN	1469-8978 ; 0033-2917
ISSN (online)	1469-8978
ISSN	0033-2917
DOI	10.1017/S0033291708004583
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Article ; Online: Schizophrenia genetics: emerging themes for a complex disorder.

Kavanagh, D H / Tansey, K E / O'Donovan, M C / Owen, M J

Molecular psychiatry

2014 Volume 20, Issue 1, Page(s) 72–76

Abstract: After two decades of frustration, genetic studies of schizophrenia have entered an era of spectacular success. Advances in genotyping technologies and high throughput sequencing, increasing analytic rigour and collaborative efforts on a global scale have ...

Abstract	After two decades of frustration, genetic studies of schizophrenia have entered an era of spectacular success. Advances in genotyping technologies and high throughput sequencing, increasing analytic rigour and collaborative efforts on a global scale have generated a profusion of new findings. The broad conclusions from these studies are threefold: (1) schizophrenia is a highly polygenic disorder with a complex array of contributing risk loci across the allelic frequency spectrum; (2) many psychiatric illnesses share risk genes and alleles, specifically, schizophrenia has substantial overlaps with bipolar disorder, intellectual disability, major depressive disorder and autism spectrum disorders; and (3) some convergent biological themes are emerging from studies of schizophrenia and related disorders. In this commentary, we focus on the very recent findings that have emerged in the past 12 months, and in particular, the areas of convergence that are beginning to emerge from multiple study designs.
MeSH term(s)	Bipolar Disorder/etiology ; Bipolar Disorder/genetics ; Gene Frequency ; Genetic Predisposition to Disease/genetics ; Genetic Variation/genetics ; Genome-Wide Association Study ; Genotype ; Humans ; Intellectual Disability/etiology ; Intellectual Disability/genetics ; Schizophrenia/complications ; Schizophrenia/genetics
Language	English
Publishing date	2014-11-11
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1330655-8
ISSN	1476-5578 ; 1359-4184
ISSN (online)	1476-5578
ISSN	1359-4184
DOI	10.1038/mp.2014.148
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Article: Psychosis genetics: modeling the relationship between schizophrenia, bipolar disorder, and mixed (or "schizoaffective") psychoses.

Craddock, Nick / O'Donovan, M C / Owen, M J

Schizophrenia bulletin

2009 Volume 35, Issue 3, Page(s) 482–490

Abstract: As a result of improving technologies and greatly increased sample sizes, the last 2 years has seen unprecedented advances in identification of specific genetic risk factors for psychiatric phenotypes. Strong genetic associations have been reported at ... ...

Abstract	As a result of improving technologies and greatly increased sample sizes, the last 2 years has seen unprecedented advances in identification of specific genetic risk factors for psychiatric phenotypes. Strong genetic associations have been reported at common polymorphisms within ANK3 and CACNA1C in bipolar disorder and ZNF804A in schizophrenia and a relatively specific association between common variation in GABA(A) receptor genes and cases with features of both bipolar disorder and schizophrenia. Further, the occurrence of rare copy number variants (CNVs) has been shown to be increased in schizophrenia compared with controls. These emerging data provide a powerful resource for exploring the relationship between psychiatric phenotypes and can, and should, be used to inform conceptualization, classification, and diagnosis in psychiatry. It is already clear that, in general, genetic associations are not specific to one of the traditional diagnostic categories. For example, variation at ZNF804A is associated with risk of both bipolar disorder and schizophrenia, and some rare CNVs are associated with risk of autism and epilepsy as well as schizophrenia. These data are not consistent with a simple dichotomous model of functional psychosis and indicate the urgent need for moves toward approaches that (a) better represent the range of phenotypic variation seen in the clinical population and (b) reflect the underlying biological variation that gives rise to the phenotypes. We consider the implications for models of psychosis and the importance of recognizing and studying illness that has prominent affective and psychotic features. We conclude that if psychiatry is to translate the opportunities offered by new research methodologies, we must finally abandon a 19th-century dichotomy and move to a classificatory approach that is worthy of the 21st century.
MeSH term(s)	Ankyrins/genetics ; Bipolar Disorder/classification ; Bipolar Disorder/diagnosis ; Bipolar Disorder/genetics ; Calcium Channels, L-Type/genetics ; Gene Dosage ; Genetic Predisposition to Disease/genetics ; Humans ; Kruppel-Like Transcription Factors/genetics ; Models, Genetic ; Phenotype ; Polymorphism, Genetic/genetics ; Psychotic Disorders/classification ; Psychotic Disorders/diagnosis ; Psychotic Disorders/genetics ; Receptors, GABA-A/genetics ; Schizophrenia/classification ; Schizophrenia/diagnosis ; Schizophrenia/genetics
Chemical Substances	ANK3 protein, human ; Ankyrins ; CACNA1C protein, human ; Calcium Channels, L-Type ; Kruppel-Like Transcription Factors ; Receptors, GABA-A ; ZNF804A protein, human
Language	English
Publishing date	2009-03-27
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	439173-1
ISSN	1745-1701 ; 0586-7614
ISSN (online)	1745-1701
ISSN	0586-7614
DOI	10.1093/schbul/sbp020
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Article ; Online: Mental disorders of known aetiology and precision medicine in psychiatry: a promising but neglected alliance.

Fraguas, D / Díaz-Caneja, C M / State, M W / O'Donovan, M C / Gur, R E / Arango, C

Psychological medicine

2016 Volume 47, Issue 2, Page(s) 193–197

Abstract: Personalized or precision medicine is predicated on the assumption that the average response to treatment is not necessarily representative of the response of each individual. A commitment to personalized medicine demands an effort to bring evidence- ... ...

Abstract	Personalized or precision medicine is predicated on the assumption that the average response to treatment is not necessarily representative of the response of each individual. A commitment to personalized medicine demands an effort to bring evidence-based medicine and personalized medicine closer together. The use of relatively homogeneous groups, defined using a priori criteria, may constitute a promising initial step for developing more accurate risk-prediction models with which to advance the development of personalized evidence-based medicine approaches to heterogeneous syndromes such as schizophrenia. However, this can lead to a paradoxical situation in the field of psychiatry. Since there has been a tendency to loosely define psychiatric disorders as ones without a known aetiology, the discovery of an aetiology for psychiatric syndromes (e.g. 22q11.2 deletion syndrome in some cases of schizophrenia), while offering a path toward more precise treatments, may also lead to their reclassification away from psychiatry. We contend that psychiatric disorders with a known aetiology should not be removed from the field of psychiatry. This knowledge should be used instead to guide treatment, inasmuch as psychotherapies, pharmacotherapies and other treatments can all be valid approaches to mental disorders. The translation of the personalized clinical approach inherent to psychiatry into evidence-based precision medicine can lead to the development of novel treatment options for mental disorders and improve outcomes.
MeSH term(s)	Humans ; Mental Disorders/etiology ; Mental Disorders/therapy ; Precision Medicine/methods ; Precision Medicine/standards ; Psychiatry/methods ; Psychiatry/standards
Language	English
Publishing date	2016-06-23
Publishing country	England
Document type	Editorial ; Research Support, Non-U.S. Gov't
ZDB-ID	217420-0
ISSN	1469-8978 ; 0033-2917
ISSN (online)	1469-8978
ISSN	0033-2917
DOI	10.1017/S0033291716001355
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Article ; Online: Genome-wide association studies in psychiatry: lessons from early studies of non-psychiatric and psychiatric phenotypes.

Craddock, N / O'Donovan, M C / Owen, M J

Molecular psychiatry

2008 Volume 13, Issue 7, Page(s) 649–653

MeSH term(s)	Complement Factor H/genetics ; Genome, Human ; Humans ; Macular Degeneration/genetics ; Mental Disorders/genetics ; Phenotype ; Polymorphism, Genetic ; Polymorphism, Single Nucleotide ; Psychotic Disorders/genetics ; Reference Values ; Research Design ; Sample Size
Chemical Substances	CFH protein, human ; Complement Factor H (80295-65-4)
Language	English
Publishing date	2008-05-27
Publishing country	England
Document type	Editorial
ZDB-ID	1330655-8
ISSN	1476-5578 ; 1359-4184
ISSN (online)	1476-5578
ISSN	1359-4184
DOI	10.1038/mp.2008.45
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