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PubMed | University of Nottingham, Queen Elizabeth Hospital, Fulbourn Hospital, Center for Neuropsychiatric Genetics and Genomics and 18 more.
Type: Journal Article | Journal: Journal of psychopharmacology (Oxford, England) | Year: 2016

The British Association for Psychopharmacology guidelines specify the scope and targets of treatment for bipolar disorder. The third version is based explicitly on the available evidence and presented, like previous Clinical Practice Guidelines, as recommendations to aid clinical decision making for practitioners: it may also serve as a source of information for patients and carers, and assist audit. The recommendations are presented together with a more detailed review of the corresponding evidence. A consensus meeting, involving experts in bipolar disorder and its treatment, reviewed key areas and considered the strength of evidence and clinical implications. The guidelines were drawn up after extensive feedback from these participants. The best evidence from randomized controlled trials and, where available, observational studies employing quasi-experimental designs was used to evaluate treatment options. The strength of recommendations has been described using the GRADE approach. The guidelines cover the diagnosis of bipolar disorder, clinical management, and strategies for the use of medicines in short-term treatment of episodes, relapse prevention and stopping treatment. The use of medication is integrated with a coherent approach to psychoeducation and behaviour change.


Schepman K.,Center for Neuropsychiatric Genetics and Genomics | Taylor E.,King's College London | Collishaw S.,Center for Neuropsychiatric Genetics and Genomics | Fombonne E.,McGill University
Journal of Abnormal Child Psychology | Year: 2012

Studies of adults with depression point to characteristic neurocognitive deficits, including differences in processing facial expressions. Few studies have examined face processing in juvenile depression, or taken account of other comorbid disorders. Three groups were compared: depressed children and adolescents with conduct disorder (n=23), depressed children and adolescents without conduct disorder (n=29) and children and adolescents without disorder (n=37). A novel face emotion processing experiment presented faces with 'happy', 'sad', 'angry', or 'fearful' expressions of varying emotional intensity using morphed stimuli. Those with depression showed no overall or specific deficits in facial expression recognition accuracy. Instead, they showed biases affecting processing of lowintensity expressions, more often perceiving these as sad. In contrast, non-depressed controls more often misperceived low intensity negative emotions as happy. There were no differences between depressed children and adolescents with and without conduct disorder, or between children with comorbid depression/conduct disorder and controls. Face emotion processing biases rather than deficits appear to distinguish depressed from non-depressed children and adolescents. © Springer Science+Business Media, LLC 2011.


Grozeva D.,Center for Neuropsychiatric Genetics and Genomics | Kirov G.,Center for Neuropsychiatric Genetics and Genomics | Conrad D.F.,Wellcome Trust Sanger Institute | Barnes C.P.,Wellcome Trust Sanger Institute | And 4 more authors.
Bipolar Disorders | Year: 2013

Objectives: Large, rare chromosomal copy number variants (CNVs) have been shown to increase the risk for schizophrenia and other neuropsychiatric disorders including autism, attention-deficit hyperactivity disorder, learning difficulties, and epilepsy. Their role in bipolar disorder (BD) is less clear. There are no reports of an increase in large, rare CNVs in BD in general, but some have reported an increase in early-onset cases. We previously found that the rate of such CNVs in individuals with BD was not increased, even in early-onset cases. Our aim here was to examine the rate of large rare CNVs in BD in comparison with a new large independent reference sample from the same country. Methods: We studied the CNVs in a case-control sample consisting of 1,650 BD cases (reported previously) and 10,259 reference individuals without a known psychiatric disorder who took part in the original Wellcome Trust Case Control Consortium (WTCCC) study. The 10,259 reference individuals were affected with six non-psychiatric disorders (coronary artery disease, types 1 and 2 diabetes, hypertension, Crohn's disease, and rheumatoid arthritis). Affymetrix 500K array genotyping data were used to call the CNVs. Results: The rate of CNVs > 100 kb was not statistically different between cases and controls. The rate of very large (defined as > 1 Mb) and rare (< 1%) CNVs was significantly lower in patients with BD compared with the reference group. CNV loci associated with schizophrenia were not enriched in BD and, in fact, cases of BD had the lowest number of such CNVs compared with any of the WTCCC cohorts; this finding held even for the early-onset BD cases. Conclusions: Schizophrenia and BD differ with respect to CNV burden and association with specific CNVs. Our findings support the hypothesis that BD is etiologically distinct from schizophrenia with respect to large, rare CNVs and the accompanying associated neurodevelopmental abnormalities. © 2013 John Wiley & Sons A/S.


Hinton E.C.,University of Cardiff | Isles A.R.,Behavioural Genetics Group | Williams N.M.,Center for Neuropsychiatric Genetics and Genomics | Parkinson J.A.,Bangor University
Appetite | Year: 2010

This study focused on genetic and behavioural aspects of one important component of the motivation to eat - how appetitive arousal is elicited through the presentation of food-associated stimuli. Individuals with Prader-Willi syndrome, a genetic disorder associated with hyperphagia, and control participants completed a computerised response task in the presence of motivational stimuli. In controls, appetitive arousal was specific to particular stimuli. In contrast, individuals with PWS showed a non-specific pattern of arousal. Over-activation of the anticipatory motivation system may be one consequence of the genetic disorder in PWS. © 2009 Elsevier Ltd. All rights reserved.


Peall K.J.,Center for Neuropsychiatric Genetics and Genomics | Waite A.J.,Center for Neuropsychiatric Genetics and Genomics | Blake D.J.,Center for Neuropsychiatric Genetics and Genomics | Owen M.J.,Center for Neuropsychiatric Genetics and Genomics | Morris H.R.,Center for Neuropsychiatric Genetics and Genomics
Movement Disorders | Year: 2011

Background: Mutations in the maternally imprinted epsilon-sarcoglycan gene occur in 30%-50% of myoclonus-dystonia cases. Psychiatric symptoms, particularly obsessive-compulsive disorder, have been described in some patients. Methods: We systematically reviewed 22 reports of psychiatric symptoms in myoclonus-dystonia, dividing individuals according to clinical and mutation status. Results: Clinically manifesting mutation carriers demonstrated an excess of psychiatric disorders compared with nonmutation carriers (P < .001). No differences were seen between non-motor-manifesting carriers and nonmutation carriers with the exception of alcohol excess/dependence, higher in non-motor-manifesting carriers. Conclusions: The results confirm the association of epsilon-sarcoglycan gene mutations with psychiatric disease and suggest a possible separation of the motor and psychiatric effects. © 2011 Movement Disorder Society.


Knott S.,Center for Neuropsychiatric Genetics and Genomics | Forty L.,Center for Neuropsychiatric Genetics and Genomics | Craddock N.,Center for Neuropsychiatric Genetics and Genomics | Thomas R.H.,Center for Neuropsychiatric Genetics and Genomics
Epilepsy and Behavior | Year: 2015

It is well recognized that mood disorders and epilepsy commonly co-occur. Despite this, our knowledge regarding the relationship between epilepsy and bipolar disorder is limited. Several shared features between the two disorders, such as their episodic nature and potential to run a chronic course, and the efficacy of some antiepileptic medications in the prophylaxis of both disorders, are often cited as evidence of possible shared underlying pathophysiology. The present paper aims to review the bidirectional associations between epilepsy and bipolar disorder, with a focus on epidemiological links, evidence for shared etiology, and the impact of these disorders on both the individual and wider society. Better recognition and understanding of these two complex disorders, along with an integrated clinical approach, are crucial for improved evaluation and management of comorbid epilepsy and mood disorders. © 2015 Elsevier Inc.


Jones L.,Center for Neuropsychiatric Genetics and Genomics | Harold D.,Center for Neuropsychiatric Genetics and Genomics | Williams J.,Center for Neuropsychiatric Genetics and Genomics
Biochimica et Biophysica Acta - Molecular and Cell Biology of Lipids | Year: 2010

Alzheimer's disease (AD) is the most common cause of dementia in the elderly and presents a great burden to sufferers and to society. The genetics of rare Mendelian forms of AD have been central to our understanding of AD pathogenesis for the past twenty years and now the genetics of the common form of the disease in the elderly is beginning to be unravelled by genome-wide association studies. Four new genes for common AD have been revealed in the past year, CLU, CR1, PICALM and BIN1. Their possible involvement in lipid metabolism and how that relates to AD is discussed here. © 2010 Elsevier B.V. All rights reserved.


PubMed | Center for Neuropsychiatric Genetics and Genomics
Type: Journal Article | Journal: Movement disorders : official journal of the Movement Disorder Society | Year: 2011

Mutations in the maternally imprinted epsilon-sarcoglycan gene occur in 30%-50% of myoclonus-dystonia cases. Psychiatric symptoms, particularly obsessive-compulsive disorder, have been described in some patients.We systematically reviewed 22 reports of psychiatric symptoms in myoclonus-dystonia, dividing individuals according to clinical and mutation status.Clinically manifesting mutation carriers demonstrated an excess of psychiatric disorders compared with nonmutation carriers (P < .001). No differences were seen between non-motor-manifesting carriers and nonmutation carriers with the exception of alcohol excess/dependence, higher in non-motor-manifesting carriers.The results confirm the association of epsilon-sarcoglycan gene mutations with psychiatric disease and suggest a possible separation of the motor and psychiatric effects.


PubMed | Center for Neuropsychiatric Genetics and Genomics
Type: Journal Article | Journal: Epilepsy & behavior : E&B | Year: 2015

It is well recognized that mood disorders and epilepsy commonly co-occur. Despite this, our knowledge regarding the relationship between epilepsy and bipolar disorder is limited. Several shared features between the two disorders, such as their episodic nature and potential to run a chronic course, and the efficacy of some antiepileptic medications in the prophylaxis of both disorders, are often cited as evidence of possible shared underlying pathophysiology. The present paper aims to review the bidirectional associations between epilepsy and bipolar disorder, with a focus on epidemiological links, evidence for shared etiology, and the impact of these disorders on both the individual and wider society. Better recognition and understanding of these two complex disorders, along with an integrated clinical approach, are crucial for improved evaluation and management of comorbid epilepsy and mood disorders.


PubMed | Center for Neuropsychiatric Genetics and Genomics
Type: Journal Article | Journal: Bipolar disorders | Year: 2013

Large, rare chromosomal copy number variants (CNVs) have been shown to increase the risk for schizophrenia and other neuropsychiatric disorders including autism, attention-deficit hyperactivity disorder, learning difficulties, and epilepsy. Their role in bipolar disorder (BD) is less clear. There are no reports of an increase in large, rare CNVs in BD in general, but some have reported an increase in early-onset cases. We previously found that the rate of such CNVs in individuals with BD was not increased, even in early-onset cases. Our aim here was to examine the rate of large rare CNVs in BD in comparison with a new large independent reference sample from the same country.We studied the CNVs in a case-control sample consisting of 1,650 BD cases (reported previously) and 10,259 reference individuals without a known psychiatric disorder who took part in the original Wellcome Trust Case Control Consortium (WTCCC) study. The 10,259 reference individuals were affected with six non-psychiatric disorders (coronary artery disease, types 1 and 2 diabetes, hypertension, Crohns disease, and rheumatoid arthritis). Affymetrix 500K array genotyping data were used to call the CNVs.The rate of CNVs > 100 kb was not statistically different between cases and controls. The rate of very large (defined as > 1 Mb) and rare (< 1%) CNVs was significantly lower in patients with BD compared with the reference group. CNV loci associated with schizophrenia were not enriched in BD and, in fact, cases of BD had the lowest number of such CNVs compared with any of the WTCCC cohorts; this finding held even for the early-onset BD cases.Schizophrenia and BD differ with respect to CNV burden and association with specific CNVs. Our findings support the hypothesis that BD is etiologically distinct from schizophrenia with respect to large, rare CNVs and the accompanying associated neurodevelopmental abnormalities.

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