The Experts below are selected from a list of 2298 Experts worldwide ranked by ideXlab platform
Marian L. Hamshere - One of the best experts on this subject based on the ideXlab platform.
-
Erratum: Strong genetic evidence for a selective influence of GABA_A receptors on a component of the bipolar disorder phenotype
Molecular Psychiatry, 2010Co-Authors: N Craddock, Marian L. Hamshere, Lisa Jones, George Kirov, Elaine K Green, Detelina Grozeva, Valentina Moskvina, Ivan Nikolov, I R Jones, D VukcevicAbstract:Correction to: Molecular Psychiatry (2010) 15, 146–153; published online 1 July 2008; doi:10.1038/mp.2008.66 In the abstract of the published version of this article it was stated that association signals were shown at GABRB1, GABRA4, GABRB3, GABRA5 and GABRR1. This last gene was stated incorrectly in the abstract and the list should have read GABRB1, GABRA4, GABRB3, GABRA5 and GABRR3, as is stated in the text.
-
Variation at the GABAA receptor gene, Rho 1 (GABRR1) associated with susceptibility to bipolar schizoaffective disorder.
American journal of medical genetics. Part B Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics, 2010Co-Authors: Elaine K Green, Marian L. Hamshere, Lisa Jones, Detelina Grozeva, Valentina Moskvina, Ian R Jones, Liz Forty, Sian Caesar, Katherine Gordon-smith, Christine FraserAbstract:We have previously reported evidence that variation at GABA(A) receptor genes is associated with susceptibility to bipolar disorder with schizophrenia-like psychotic features (Research Diagnostic Criteria (RDC) schizoaffective disorder, bipolar type) with gene-wide significance at GABRB1, GABRA4, GABRB3, GABRA5, and GABRR3. Here we provide suggestive evidence implicating a sixth member of the gene family, GABRR1 (gene-wide P = 0.0058; experiment-wide corrected significance P = 0.052).
-
Strong genetic evidence for a selective influence of GABAA receptors on a component of the bipolar disorder phenotype [Corrigendum]
Molecular Psychiatry, 2010Co-Authors: Nicholas John Craddock, Marian L. Hamshere, Ian Jones, George Kirov, Elaine K Green, Detelina Grozeva, Ivan Nikolov, Lesley Jones, Valentina Escott-price, D VukcevicAbstract:Correction to: Molecular Psychiatry (2010) 15, 146–153; published online 1 July 2008; doi:10.1038/mp.2008.66 In the abstract of the published version of this article it was stated that association signals were shown at GABRB1, GABRA4, GABRB3, GABRA5 and GABRR1. This last gene was stated incorrectly in the abstract and the list should have read GABRB1, GABRA4, GABRB3, GABRA5 and GABRR3, as is stated in the text.
-
strong genetic evidence for a selective influence of gabaa receptors on a component of the bipolar disorder phenotype
Molecular Psychiatry, 2010Co-Authors: Nicholas John Craddock, Marian L. Hamshere, Lisa Jones, Ian Jones, George Kirov, Elaine K Green, Detelina Grozeva, Valentina Moskvina, Ivan NikolovAbstract:Despite compelling evidence for a major genetic contribution to risk of bipolar mood disorder, conclusive evidence implicating specific genes or pathophysiological systems has proved elusive. In part this is likely to be related to the unknown validity of current phenotype definitions and consequent aetiological heterogeneity of samples. In the recent Wellcome Trust Case Control Consortium genome-wide association analysis of bipolar disorder (1868 cases, 2938 controls) one of the most strongly associated polymorphisms lay within the gene encoding the GABAA receptor β1 subunit, GABRB1. Aiming to increase biological homogeneity, we sought the diagnostic subset that showed the strongest signal at this polymorphism and used this to test for independent evidence of association with other members of the GABAA receptor gene family. The index signal was significantly enriched in the 279 cases meeting Research Diagnostic Criteria for schizoaffective disorder, bipolar type (P=3.8 × 10−6). Independently, these cases showed strong evidence that variation in GABAA receptor genes influences risk for this phenotype (independent system-wide P=6.6 × 10−5) with association signals also at GABRA4, GABRB3, GABRA5 and GABRR1. Our findings have the potential to inform understanding of presentation, pathogenesis and nosology of bipolar disorders. Our method of phenotype refinement may be useful in studies of other complex psychiatric and non-psychiatric disorders.
Elaine K Green - One of the best experts on this subject based on the ideXlab platform.
-
Erratum: Strong genetic evidence for a selective influence of GABA_A receptors on a component of the bipolar disorder phenotype
Molecular Psychiatry, 2010Co-Authors: N Craddock, Marian L. Hamshere, Lisa Jones, George Kirov, Elaine K Green, Detelina Grozeva, Valentina Moskvina, Ivan Nikolov, I R Jones, D VukcevicAbstract:Correction to: Molecular Psychiatry (2010) 15, 146–153; published online 1 July 2008; doi:10.1038/mp.2008.66 In the abstract of the published version of this article it was stated that association signals were shown at GABRB1, GABRA4, GABRB3, GABRA5 and GABRR1. This last gene was stated incorrectly in the abstract and the list should have read GABRB1, GABRA4, GABRB3, GABRA5 and GABRR3, as is stated in the text.
-
Variation at the GABAA receptor gene, Rho 1 (GABRR1) associated with susceptibility to bipolar schizoaffective disorder.
American journal of medical genetics. Part B Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics, 2010Co-Authors: Elaine K Green, Marian L. Hamshere, Lisa Jones, Detelina Grozeva, Valentina Moskvina, Ian R Jones, Liz Forty, Sian Caesar, Katherine Gordon-smith, Christine FraserAbstract:We have previously reported evidence that variation at GABA(A) receptor genes is associated with susceptibility to bipolar disorder with schizophrenia-like psychotic features (Research Diagnostic Criteria (RDC) schizoaffective disorder, bipolar type) with gene-wide significance at GABRB1, GABRA4, GABRB3, GABRA5, and GABRR3. Here we provide suggestive evidence implicating a sixth member of the gene family, GABRR1 (gene-wide P = 0.0058; experiment-wide corrected significance P = 0.052).
-
Strong genetic evidence for a selective influence of GABAA receptors on a component of the bipolar disorder phenotype [Corrigendum]
Molecular Psychiatry, 2010Co-Authors: Nicholas John Craddock, Marian L. Hamshere, Ian Jones, George Kirov, Elaine K Green, Detelina Grozeva, Ivan Nikolov, Lesley Jones, Valentina Escott-price, D VukcevicAbstract:Correction to: Molecular Psychiatry (2010) 15, 146–153; published online 1 July 2008; doi:10.1038/mp.2008.66 In the abstract of the published version of this article it was stated that association signals were shown at GABRB1, GABRA4, GABRB3, GABRA5 and GABRR1. This last gene was stated incorrectly in the abstract and the list should have read GABRB1, GABRA4, GABRB3, GABRA5 and GABRR3, as is stated in the text.
-
strong genetic evidence for a selective influence of gabaa receptors on a component of the bipolar disorder phenotype
Molecular Psychiatry, 2010Co-Authors: Nicholas John Craddock, Marian L. Hamshere, Lisa Jones, Ian Jones, George Kirov, Elaine K Green, Detelina Grozeva, Valentina Moskvina, Ivan NikolovAbstract:Despite compelling evidence for a major genetic contribution to risk of bipolar mood disorder, conclusive evidence implicating specific genes or pathophysiological systems has proved elusive. In part this is likely to be related to the unknown validity of current phenotype definitions and consequent aetiological heterogeneity of samples. In the recent Wellcome Trust Case Control Consortium genome-wide association analysis of bipolar disorder (1868 cases, 2938 controls) one of the most strongly associated polymorphisms lay within the gene encoding the GABAA receptor β1 subunit, GABRB1. Aiming to increase biological homogeneity, we sought the diagnostic subset that showed the strongest signal at this polymorphism and used this to test for independent evidence of association with other members of the GABAA receptor gene family. The index signal was significantly enriched in the 279 cases meeting Research Diagnostic Criteria for schizoaffective disorder, bipolar type (P=3.8 × 10−6). Independently, these cases showed strong evidence that variation in GABAA receptor genes influences risk for this phenotype (independent system-wide P=6.6 × 10−5) with association signals also at GABRA4, GABRB3, GABRA5 and GABRR1. Our findings have the potential to inform understanding of presentation, pathogenesis and nosology of bipolar disorders. Our method of phenotype refinement may be useful in studies of other complex psychiatric and non-psychiatric disorders.
Detelina Grozeva - One of the best experts on this subject based on the ideXlab platform.
-
Erratum: Strong genetic evidence for a selective influence of GABA_A receptors on a component of the bipolar disorder phenotype
Molecular Psychiatry, 2010Co-Authors: N Craddock, Marian L. Hamshere, Lisa Jones, George Kirov, Elaine K Green, Detelina Grozeva, Valentina Moskvina, Ivan Nikolov, I R Jones, D VukcevicAbstract:Correction to: Molecular Psychiatry (2010) 15, 146–153; published online 1 July 2008; doi:10.1038/mp.2008.66 In the abstract of the published version of this article it was stated that association signals were shown at GABRB1, GABRA4, GABRB3, GABRA5 and GABRR1. This last gene was stated incorrectly in the abstract and the list should have read GABRB1, GABRA4, GABRB3, GABRA5 and GABRR3, as is stated in the text.
-
Variation at the GABAA receptor gene, Rho 1 (GABRR1) associated with susceptibility to bipolar schizoaffective disorder.
American journal of medical genetics. Part B Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics, 2010Co-Authors: Elaine K Green, Marian L. Hamshere, Lisa Jones, Detelina Grozeva, Valentina Moskvina, Ian R Jones, Liz Forty, Sian Caesar, Katherine Gordon-smith, Christine FraserAbstract:We have previously reported evidence that variation at GABA(A) receptor genes is associated with susceptibility to bipolar disorder with schizophrenia-like psychotic features (Research Diagnostic Criteria (RDC) schizoaffective disorder, bipolar type) with gene-wide significance at GABRB1, GABRA4, GABRB3, GABRA5, and GABRR3. Here we provide suggestive evidence implicating a sixth member of the gene family, GABRR1 (gene-wide P = 0.0058; experiment-wide corrected significance P = 0.052).
-
Strong genetic evidence for a selective influence of GABAA receptors on a component of the bipolar disorder phenotype [Corrigendum]
Molecular Psychiatry, 2010Co-Authors: Nicholas John Craddock, Marian L. Hamshere, Ian Jones, George Kirov, Elaine K Green, Detelina Grozeva, Ivan Nikolov, Lesley Jones, Valentina Escott-price, D VukcevicAbstract:Correction to: Molecular Psychiatry (2010) 15, 146–153; published online 1 July 2008; doi:10.1038/mp.2008.66 In the abstract of the published version of this article it was stated that association signals were shown at GABRB1, GABRA4, GABRB3, GABRA5 and GABRR1. This last gene was stated incorrectly in the abstract and the list should have read GABRB1, GABRA4, GABRB3, GABRA5 and GABRR3, as is stated in the text.
-
strong genetic evidence for a selective influence of gabaa receptors on a component of the bipolar disorder phenotype
Molecular Psychiatry, 2010Co-Authors: Nicholas John Craddock, Marian L. Hamshere, Lisa Jones, Ian Jones, George Kirov, Elaine K Green, Detelina Grozeva, Valentina Moskvina, Ivan NikolovAbstract:Despite compelling evidence for a major genetic contribution to risk of bipolar mood disorder, conclusive evidence implicating specific genes or pathophysiological systems has proved elusive. In part this is likely to be related to the unknown validity of current phenotype definitions and consequent aetiological heterogeneity of samples. In the recent Wellcome Trust Case Control Consortium genome-wide association analysis of bipolar disorder (1868 cases, 2938 controls) one of the most strongly associated polymorphisms lay within the gene encoding the GABAA receptor β1 subunit, GABRB1. Aiming to increase biological homogeneity, we sought the diagnostic subset that showed the strongest signal at this polymorphism and used this to test for independent evidence of association with other members of the GABAA receptor gene family. The index signal was significantly enriched in the 279 cases meeting Research Diagnostic Criteria for schizoaffective disorder, bipolar type (P=3.8 × 10−6). Independently, these cases showed strong evidence that variation in GABAA receptor genes influences risk for this phenotype (independent system-wide P=6.6 × 10−5) with association signals also at GABRA4, GABRB3, GABRA5 and GABRR1. Our findings have the potential to inform understanding of presentation, pathogenesis and nosology of bipolar disorders. Our method of phenotype refinement may be useful in studies of other complex psychiatric and non-psychiatric disorders.
D Vukcevic - One of the best experts on this subject based on the ideXlab platform.
-
Erratum: Strong genetic evidence for a selective influence of GABA_A receptors on a component of the bipolar disorder phenotype
Molecular Psychiatry, 2010Co-Authors: N Craddock, Marian L. Hamshere, Lisa Jones, George Kirov, Elaine K Green, Detelina Grozeva, Valentina Moskvina, Ivan Nikolov, I R Jones, D VukcevicAbstract:Correction to: Molecular Psychiatry (2010) 15, 146–153; published online 1 July 2008; doi:10.1038/mp.2008.66 In the abstract of the published version of this article it was stated that association signals were shown at GABRB1, GABRA4, GABRB3, GABRA5 and GABRR1. This last gene was stated incorrectly in the abstract and the list should have read GABRB1, GABRA4, GABRB3, GABRA5 and GABRR3, as is stated in the text.
-
Strong genetic evidence for a selective influence of GABAA receptors on a component of the bipolar disorder phenotype [Corrigendum]
Molecular Psychiatry, 2010Co-Authors: Nicholas John Craddock, Marian L. Hamshere, Ian Jones, George Kirov, Elaine K Green, Detelina Grozeva, Ivan Nikolov, Lesley Jones, Valentina Escott-price, D VukcevicAbstract:Correction to: Molecular Psychiatry (2010) 15, 146–153; published online 1 July 2008; doi:10.1038/mp.2008.66 In the abstract of the published version of this article it was stated that association signals were shown at GABRB1, GABRA4, GABRB3, GABRA5 and GABRR1. This last gene was stated incorrectly in the abstract and the list should have read GABRB1, GABRA4, GABRB3, GABRA5 and GABRR3, as is stated in the text.
Nicholas John Craddock - One of the best experts on this subject based on the ideXlab platform.
-
Strong genetic evidence for a selective influence of GABAA receptors on a component of the bipolar disorder phenotype [Corrigendum]
Molecular Psychiatry, 2010Co-Authors: Nicholas John Craddock, Marian L. Hamshere, Ian Jones, George Kirov, Elaine K Green, Detelina Grozeva, Ivan Nikolov, Lesley Jones, Valentina Escott-price, D VukcevicAbstract:Correction to: Molecular Psychiatry (2010) 15, 146–153; published online 1 July 2008; doi:10.1038/mp.2008.66 In the abstract of the published version of this article it was stated that association signals were shown at GABRB1, GABRA4, GABRB3, GABRA5 and GABRR1. This last gene was stated incorrectly in the abstract and the list should have read GABRB1, GABRA4, GABRB3, GABRA5 and GABRR3, as is stated in the text.
-
strong genetic evidence for a selective influence of gabaa receptors on a component of the bipolar disorder phenotype
Molecular Psychiatry, 2010Co-Authors: Nicholas John Craddock, Marian L. Hamshere, Lisa Jones, Ian Jones, George Kirov, Elaine K Green, Detelina Grozeva, Valentina Moskvina, Ivan NikolovAbstract:Despite compelling evidence for a major genetic contribution to risk of bipolar mood disorder, conclusive evidence implicating specific genes or pathophysiological systems has proved elusive. In part this is likely to be related to the unknown validity of current phenotype definitions and consequent aetiological heterogeneity of samples. In the recent Wellcome Trust Case Control Consortium genome-wide association analysis of bipolar disorder (1868 cases, 2938 controls) one of the most strongly associated polymorphisms lay within the gene encoding the GABAA receptor β1 subunit, GABRB1. Aiming to increase biological homogeneity, we sought the diagnostic subset that showed the strongest signal at this polymorphism and used this to test for independent evidence of association with other members of the GABAA receptor gene family. The index signal was significantly enriched in the 279 cases meeting Research Diagnostic Criteria for schizoaffective disorder, bipolar type (P=3.8 × 10−6). Independently, these cases showed strong evidence that variation in GABAA receptor genes influences risk for this phenotype (independent system-wide P=6.6 × 10−5) with association signals also at GABRA4, GABRB3, GABRA5 and GABRR1. Our findings have the potential to inform understanding of presentation, pathogenesis and nosology of bipolar disorders. Our method of phenotype refinement may be useful in studies of other complex psychiatric and non-psychiatric disorders.