Identification of shared risk loci and pathways for bipolar disorder and schizophrenia.
Bipolar disorder (BD) is a highly heritable neuropsychiatric disease characterized by recurrent episodes of mania and depression. BD shows substantial clinical and genetic overlap with other psychiatric disorders, in particular schizophrenia (SCZ). The genes underlying this etiological overlap remai...
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Englisch |
| Erschienen: |
2017 |
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In: PLoS ONE - Public Library of Science (PLoS), 2007, 12(2017), 2, p e0171595 |
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| Übergeordnetes Werk: |
volume:12 ; year:2017 ; number:2, p e0171595 |
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| DOI / URN: |
10.1371/journal.pone.0171595 |
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DOAJ036492051 |
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| 520 | |a Bipolar disorder (BD) is a highly heritable neuropsychiatric disease characterized by recurrent episodes of mania and depression. BD shows substantial clinical and genetic overlap with other psychiatric disorders, in particular schizophrenia (SCZ). The genes underlying this etiological overlap remain largely unknown. A recent SCZ genome wide association study (GWAS) by the Psychiatric Genomics Consortium identified 128 independent genome-wide significant single nucleotide polymorphisms (SNPs). The present study investigated whether these SCZ-associated SNPs also contribute to BD development through the performance of association testing in a large BD GWAS dataset (9747 patients, 14278 controls). After re-imputation and correction for sample overlap, 22 of 107 investigated SCZ SNPs showed nominal association with BD. The number of shared SCZ-BD SNPs was significantly higher than expected (p = 1.46x10-8). This provides further evidence that SCZ-associated loci contribute to the development of BD. Two SNPs remained significant after Bonferroni correction. The most strongly associated SNP was located near TRANK1, which is a reported genome-wide significant risk gene for BD. Pathway analyses for all shared SCZ-BD SNPs revealed 25 nominally enriched gene-sets, which showed partial overlap in terms of the underlying genes. The enriched gene-sets included calcium- and glutamate signaling, neuropathic pain signaling in dorsal horn neurons, and calmodulin binding. The present data provide further insights into shared risk loci and disease-associated pathways for BD and SCZ. This may suggest new research directions for the treatment and prevention of these two major psychiatric disorders. | ||
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10.1371/journal.pone.0171595 doi (DE-627)DOAJ036492051 (DE-599)DOAJfefac7becf554988a67a692f7dcea992 DE-627 ger DE-627 rakwb eng Andreas J Forstner verfasserin aut Identification of shared risk loci and pathways for bipolar disorder and schizophrenia. 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Bipolar disorder (BD) is a highly heritable neuropsychiatric disease characterized by recurrent episodes of mania and depression. BD shows substantial clinical and genetic overlap with other psychiatric disorders, in particular schizophrenia (SCZ). The genes underlying this etiological overlap remain largely unknown. A recent SCZ genome wide association study (GWAS) by the Psychiatric Genomics Consortium identified 128 independent genome-wide significant single nucleotide polymorphisms (SNPs). The present study investigated whether these SCZ-associated SNPs also contribute to BD development through the performance of association testing in a large BD GWAS dataset (9747 patients, 14278 controls). After re-imputation and correction for sample overlap, 22 of 107 investigated SCZ SNPs showed nominal association with BD. The number of shared SCZ-BD SNPs was significantly higher than expected (p = 1.46x10-8). This provides further evidence that SCZ-associated loci contribute to the development of BD. Two SNPs remained significant after Bonferroni correction. The most strongly associated SNP was located near TRANK1, which is a reported genome-wide significant risk gene for BD. Pathway analyses for all shared SCZ-BD SNPs revealed 25 nominally enriched gene-sets, which showed partial overlap in terms of the underlying genes. The enriched gene-sets included calcium- and glutamate signaling, neuropathic pain signaling in dorsal horn neurons, and calmodulin binding. The present data provide further insights into shared risk loci and disease-associated pathways for BD and SCZ. This may suggest new research directions for the treatment and prevention of these two major psychiatric disorders. Medicine R Science Q Julian Hecker verfasserin aut Andrea Hofmann verfasserin aut Anna Maaser verfasserin aut Céline S Reinbold verfasserin aut Thomas W Mühleisen verfasserin aut Markus Leber verfasserin aut Jana Strohmaier verfasserin aut Franziska Degenhardt verfasserin aut Jens Treutlein verfasserin aut Manuel Mattheisen verfasserin aut Johannes Schumacher verfasserin aut Fabian Streit verfasserin aut Sandra Meier verfasserin aut Stefan Herms verfasserin aut Per Hoffmann verfasserin aut André Lacour verfasserin aut Stephanie H Witt verfasserin aut Andreas Reif verfasserin aut Bertram Müller-Myhsok verfasserin aut Susanne Lucae verfasserin aut Wolfgang Maier verfasserin aut Markus Schwarz verfasserin aut Helmut Vedder verfasserin aut Jutta Kammerer-Ciernioch verfasserin aut Andrea Pfennig verfasserin aut Michael Bauer verfasserin aut Martin Hautzinger verfasserin aut Susanne Moebus verfasserin aut Lorena M Schenk verfasserin aut Sascha B Fischer verfasserin aut Sugirthan Sivalingam verfasserin aut Piotr M Czerski verfasserin aut Joanna Hauser verfasserin aut Jolanta Lissowska verfasserin aut Neonila Szeszenia-Dabrowska verfasserin aut Paul Brennan verfasserin aut James D McKay verfasserin aut Adam Wright verfasserin aut Philip B Mitchell verfasserin aut Janice M Fullerton verfasserin aut Peter R Schofield verfasserin aut Grant W Montgomery verfasserin aut Sarah E Medland verfasserin aut Scott D Gordon verfasserin aut Nicholas G Martin verfasserin aut Valery Krasnov verfasserin aut Alexander Chuchalin verfasserin aut Gulja Babadjanova verfasserin aut Galina Pantelejeva verfasserin aut Lilia I Abramova verfasserin aut Alexander S Tiganov verfasserin aut Alexey Polonikov verfasserin aut Elza Khusnutdinova verfasserin aut Martin Alda verfasserin aut Cristiana Cruceanu verfasserin aut Guy A Rouleau verfasserin aut Gustavo Turecki verfasserin aut Catherine Laprise verfasserin aut Fabio Rivas verfasserin aut Fermin Mayoral verfasserin aut Manolis Kogevinas verfasserin aut Maria Grigoroiu-Serbanescu verfasserin aut Tim Becker verfasserin aut Thomas G Schulze verfasserin aut Marcella Rietschel verfasserin aut Sven Cichon verfasserin aut Heide Fier verfasserin aut Markus M Nöthen verfasserin aut In PLoS ONE Public Library of Science (PLoS), 2007 12(2017), 2, p e0171595 (DE-627)523574592 (DE-600)2267670-3 19326203 nnns volume:12 year:2017 number:2, p e0171595 https://doi.org/10.1371/journal.pone.0171595 kostenfrei https://doaj.org/article/fefac7becf554988a67a692f7dcea992 kostenfrei http://europepmc.org/articles/PMC5293228?pdf=render kostenfrei https://doaj.org/toc/1932-6203 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_34 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_235 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 12 2017 2, p e0171595 |
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10.1371/journal.pone.0171595 doi (DE-627)DOAJ036492051 (DE-599)DOAJfefac7becf554988a67a692f7dcea992 DE-627 ger DE-627 rakwb eng Andreas J Forstner verfasserin aut Identification of shared risk loci and pathways for bipolar disorder and schizophrenia. 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Bipolar disorder (BD) is a highly heritable neuropsychiatric disease characterized by recurrent episodes of mania and depression. BD shows substantial clinical and genetic overlap with other psychiatric disorders, in particular schizophrenia (SCZ). The genes underlying this etiological overlap remain largely unknown. A recent SCZ genome wide association study (GWAS) by the Psychiatric Genomics Consortium identified 128 independent genome-wide significant single nucleotide polymorphisms (SNPs). The present study investigated whether these SCZ-associated SNPs also contribute to BD development through the performance of association testing in a large BD GWAS dataset (9747 patients, 14278 controls). After re-imputation and correction for sample overlap, 22 of 107 investigated SCZ SNPs showed nominal association with BD. The number of shared SCZ-BD SNPs was significantly higher than expected (p = 1.46x10-8). This provides further evidence that SCZ-associated loci contribute to the development of BD. Two SNPs remained significant after Bonferroni correction. The most strongly associated SNP was located near TRANK1, which is a reported genome-wide significant risk gene for BD. Pathway analyses for all shared SCZ-BD SNPs revealed 25 nominally enriched gene-sets, which showed partial overlap in terms of the underlying genes. The enriched gene-sets included calcium- and glutamate signaling, neuropathic pain signaling in dorsal horn neurons, and calmodulin binding. The present data provide further insights into shared risk loci and disease-associated pathways for BD and SCZ. This may suggest new research directions for the treatment and prevention of these two major psychiatric disorders. Medicine R Science Q Julian Hecker verfasserin aut Andrea Hofmann verfasserin aut Anna Maaser verfasserin aut Céline S Reinbold verfasserin aut Thomas W Mühleisen verfasserin aut Markus Leber verfasserin aut Jana Strohmaier verfasserin aut Franziska Degenhardt verfasserin aut Jens Treutlein verfasserin aut Manuel Mattheisen verfasserin aut Johannes Schumacher verfasserin aut Fabian Streit verfasserin aut Sandra Meier verfasserin aut Stefan Herms verfasserin aut Per Hoffmann verfasserin aut André Lacour verfasserin aut Stephanie H Witt verfasserin aut Andreas Reif verfasserin aut Bertram Müller-Myhsok verfasserin aut Susanne Lucae verfasserin aut Wolfgang Maier verfasserin aut Markus Schwarz verfasserin aut Helmut Vedder verfasserin aut Jutta Kammerer-Ciernioch verfasserin aut Andrea Pfennig verfasserin aut Michael Bauer verfasserin aut Martin Hautzinger verfasserin aut Susanne Moebus verfasserin aut Lorena M Schenk verfasserin aut Sascha B Fischer verfasserin aut Sugirthan Sivalingam verfasserin aut Piotr M Czerski verfasserin aut Joanna Hauser verfasserin aut Jolanta Lissowska verfasserin aut Neonila Szeszenia-Dabrowska verfasserin aut Paul Brennan verfasserin aut James D McKay verfasserin aut Adam Wright verfasserin aut Philip B Mitchell verfasserin aut Janice M Fullerton verfasserin aut Peter R Schofield verfasserin aut Grant W Montgomery verfasserin aut Sarah E Medland verfasserin aut Scott D Gordon verfasserin aut Nicholas G Martin verfasserin aut Valery Krasnov verfasserin aut Alexander Chuchalin verfasserin aut Gulja Babadjanova verfasserin aut Galina Pantelejeva verfasserin aut Lilia I Abramova verfasserin aut Alexander S Tiganov verfasserin aut Alexey Polonikov verfasserin aut Elza Khusnutdinova verfasserin aut Martin Alda verfasserin aut Cristiana Cruceanu verfasserin aut Guy A Rouleau verfasserin aut Gustavo Turecki verfasserin aut Catherine Laprise verfasserin aut Fabio Rivas verfasserin aut Fermin Mayoral verfasserin aut Manolis Kogevinas verfasserin aut Maria Grigoroiu-Serbanescu verfasserin aut Tim Becker verfasserin aut Thomas G Schulze verfasserin aut Marcella Rietschel verfasserin aut Sven Cichon verfasserin aut Heide Fier verfasserin aut Markus M Nöthen verfasserin aut In PLoS ONE Public Library of Science (PLoS), 2007 12(2017), 2, p e0171595 (DE-627)523574592 (DE-600)2267670-3 19326203 nnns volume:12 year:2017 number:2, p e0171595 https://doi.org/10.1371/journal.pone.0171595 kostenfrei https://doaj.org/article/fefac7becf554988a67a692f7dcea992 kostenfrei http://europepmc.org/articles/PMC5293228?pdf=render kostenfrei https://doaj.org/toc/1932-6203 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_34 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_235 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 12 2017 2, p e0171595 |
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10.1371/journal.pone.0171595 doi (DE-627)DOAJ036492051 (DE-599)DOAJfefac7becf554988a67a692f7dcea992 DE-627 ger DE-627 rakwb eng Andreas J Forstner verfasserin aut Identification of shared risk loci and pathways for bipolar disorder and schizophrenia. 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Bipolar disorder (BD) is a highly heritable neuropsychiatric disease characterized by recurrent episodes of mania and depression. BD shows substantial clinical and genetic overlap with other psychiatric disorders, in particular schizophrenia (SCZ). The genes underlying this etiological overlap remain largely unknown. A recent SCZ genome wide association study (GWAS) by the Psychiatric Genomics Consortium identified 128 independent genome-wide significant single nucleotide polymorphisms (SNPs). The present study investigated whether these SCZ-associated SNPs also contribute to BD development through the performance of association testing in a large BD GWAS dataset (9747 patients, 14278 controls). After re-imputation and correction for sample overlap, 22 of 107 investigated SCZ SNPs showed nominal association with BD. The number of shared SCZ-BD SNPs was significantly higher than expected (p = 1.46x10-8). This provides further evidence that SCZ-associated loci contribute to the development of BD. Two SNPs remained significant after Bonferroni correction. The most strongly associated SNP was located near TRANK1, which is a reported genome-wide significant risk gene for BD. Pathway analyses for all shared SCZ-BD SNPs revealed 25 nominally enriched gene-sets, which showed partial overlap in terms of the underlying genes. The enriched gene-sets included calcium- and glutamate signaling, neuropathic pain signaling in dorsal horn neurons, and calmodulin binding. The present data provide further insights into shared risk loci and disease-associated pathways for BD and SCZ. This may suggest new research directions for the treatment and prevention of these two major psychiatric disorders. Medicine R Science Q Julian Hecker verfasserin aut Andrea Hofmann verfasserin aut Anna Maaser verfasserin aut Céline S Reinbold verfasserin aut Thomas W Mühleisen verfasserin aut Markus Leber verfasserin aut Jana Strohmaier verfasserin aut Franziska Degenhardt verfasserin aut Jens Treutlein verfasserin aut Manuel Mattheisen verfasserin aut Johannes Schumacher verfasserin aut Fabian Streit verfasserin aut Sandra Meier verfasserin aut Stefan Herms verfasserin aut Per Hoffmann verfasserin aut André Lacour verfasserin aut Stephanie H Witt verfasserin aut Andreas Reif verfasserin aut Bertram Müller-Myhsok verfasserin aut Susanne Lucae verfasserin aut Wolfgang Maier verfasserin aut Markus Schwarz verfasserin aut Helmut Vedder verfasserin aut Jutta Kammerer-Ciernioch verfasserin aut Andrea Pfennig verfasserin aut Michael Bauer verfasserin aut Martin Hautzinger verfasserin aut Susanne Moebus verfasserin aut Lorena M Schenk verfasserin aut Sascha B Fischer verfasserin aut Sugirthan Sivalingam verfasserin aut Piotr M Czerski verfasserin aut Joanna Hauser verfasserin aut Jolanta Lissowska verfasserin aut Neonila Szeszenia-Dabrowska verfasserin aut Paul Brennan verfasserin aut James D McKay verfasserin aut Adam Wright verfasserin aut Philip B Mitchell verfasserin aut Janice M Fullerton verfasserin aut Peter R Schofield verfasserin aut Grant W Montgomery verfasserin aut Sarah E Medland verfasserin aut Scott D Gordon verfasserin aut Nicholas G Martin verfasserin aut Valery Krasnov verfasserin aut Alexander Chuchalin verfasserin aut Gulja Babadjanova verfasserin aut Galina Pantelejeva verfasserin aut Lilia I Abramova verfasserin aut Alexander S Tiganov verfasserin aut Alexey Polonikov verfasserin aut Elza Khusnutdinova verfasserin aut Martin Alda verfasserin aut Cristiana Cruceanu verfasserin aut Guy A Rouleau verfasserin aut Gustavo Turecki verfasserin aut Catherine Laprise verfasserin aut Fabio Rivas verfasserin aut Fermin Mayoral verfasserin aut Manolis Kogevinas verfasserin aut Maria Grigoroiu-Serbanescu verfasserin aut Tim Becker verfasserin aut Thomas G Schulze verfasserin aut Marcella Rietschel verfasserin aut Sven Cichon verfasserin aut Heide Fier verfasserin aut Markus M Nöthen verfasserin aut In PLoS ONE Public Library of Science (PLoS), 2007 12(2017), 2, p e0171595 (DE-627)523574592 (DE-600)2267670-3 19326203 nnns volume:12 year:2017 number:2, p e0171595 https://doi.org/10.1371/journal.pone.0171595 kostenfrei https://doaj.org/article/fefac7becf554988a67a692f7dcea992 kostenfrei http://europepmc.org/articles/PMC5293228?pdf=render kostenfrei https://doaj.org/toc/1932-6203 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_34 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_235 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 12 2017 2, p e0171595 |
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10.1371/journal.pone.0171595 doi (DE-627)DOAJ036492051 (DE-599)DOAJfefac7becf554988a67a692f7dcea992 DE-627 ger DE-627 rakwb eng Andreas J Forstner verfasserin aut Identification of shared risk loci and pathways for bipolar disorder and schizophrenia. 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Bipolar disorder (BD) is a highly heritable neuropsychiatric disease characterized by recurrent episodes of mania and depression. BD shows substantial clinical and genetic overlap with other psychiatric disorders, in particular schizophrenia (SCZ). The genes underlying this etiological overlap remain largely unknown. A recent SCZ genome wide association study (GWAS) by the Psychiatric Genomics Consortium identified 128 independent genome-wide significant single nucleotide polymorphisms (SNPs). The present study investigated whether these SCZ-associated SNPs also contribute to BD development through the performance of association testing in a large BD GWAS dataset (9747 patients, 14278 controls). After re-imputation and correction for sample overlap, 22 of 107 investigated SCZ SNPs showed nominal association with BD. The number of shared SCZ-BD SNPs was significantly higher than expected (p = 1.46x10-8). This provides further evidence that SCZ-associated loci contribute to the development of BD. Two SNPs remained significant after Bonferroni correction. The most strongly associated SNP was located near TRANK1, which is a reported genome-wide significant risk gene for BD. Pathway analyses for all shared SCZ-BD SNPs revealed 25 nominally enriched gene-sets, which showed partial overlap in terms of the underlying genes. The enriched gene-sets included calcium- and glutamate signaling, neuropathic pain signaling in dorsal horn neurons, and calmodulin binding. The present data provide further insights into shared risk loci and disease-associated pathways for BD and SCZ. This may suggest new research directions for the treatment and prevention of these two major psychiatric disorders. Medicine R Science Q Julian Hecker verfasserin aut Andrea Hofmann verfasserin aut Anna Maaser verfasserin aut Céline S Reinbold verfasserin aut Thomas W Mühleisen verfasserin aut Markus Leber verfasserin aut Jana Strohmaier verfasserin aut Franziska Degenhardt verfasserin aut Jens Treutlein verfasserin aut Manuel Mattheisen verfasserin aut Johannes Schumacher verfasserin aut Fabian Streit verfasserin aut Sandra Meier verfasserin aut Stefan Herms verfasserin aut Per Hoffmann verfasserin aut André Lacour verfasserin aut Stephanie H Witt verfasserin aut Andreas Reif verfasserin aut Bertram Müller-Myhsok verfasserin aut Susanne Lucae verfasserin aut Wolfgang Maier verfasserin aut Markus Schwarz verfasserin aut Helmut Vedder verfasserin aut Jutta Kammerer-Ciernioch verfasserin aut Andrea Pfennig verfasserin aut Michael Bauer verfasserin aut Martin Hautzinger verfasserin aut Susanne Moebus verfasserin aut Lorena M Schenk verfasserin aut Sascha B Fischer verfasserin aut Sugirthan Sivalingam verfasserin aut Piotr M Czerski verfasserin aut Joanna Hauser verfasserin aut Jolanta Lissowska verfasserin aut Neonila Szeszenia-Dabrowska verfasserin aut Paul Brennan verfasserin aut James D McKay verfasserin aut Adam Wright verfasserin aut Philip B Mitchell verfasserin aut Janice M Fullerton verfasserin aut Peter R Schofield verfasserin aut Grant W Montgomery verfasserin aut Sarah E Medland verfasserin aut Scott D Gordon verfasserin aut Nicholas G Martin verfasserin aut Valery Krasnov verfasserin aut Alexander Chuchalin verfasserin aut Gulja Babadjanova verfasserin aut Galina Pantelejeva verfasserin aut Lilia I Abramova verfasserin aut Alexander S Tiganov verfasserin aut Alexey Polonikov verfasserin aut Elza Khusnutdinova verfasserin aut Martin Alda verfasserin aut Cristiana Cruceanu verfasserin aut Guy A Rouleau verfasserin aut Gustavo Turecki verfasserin aut Catherine Laprise verfasserin aut Fabio Rivas verfasserin aut Fermin Mayoral verfasserin aut Manolis Kogevinas verfasserin aut Maria Grigoroiu-Serbanescu verfasserin aut Tim Becker verfasserin aut Thomas G Schulze verfasserin aut Marcella Rietschel verfasserin aut Sven Cichon verfasserin aut Heide Fier verfasserin aut Markus M Nöthen verfasserin aut In PLoS ONE Public Library of Science (PLoS), 2007 12(2017), 2, p e0171595 (DE-627)523574592 (DE-600)2267670-3 19326203 nnns volume:12 year:2017 number:2, p e0171595 https://doi.org/10.1371/journal.pone.0171595 kostenfrei https://doaj.org/article/fefac7becf554988a67a692f7dcea992 kostenfrei http://europepmc.org/articles/PMC5293228?pdf=render kostenfrei https://doaj.org/toc/1932-6203 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_34 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_235 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 12 2017 2, p e0171595 |
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10.1371/journal.pone.0171595 doi (DE-627)DOAJ036492051 (DE-599)DOAJfefac7becf554988a67a692f7dcea992 DE-627 ger DE-627 rakwb eng Andreas J Forstner verfasserin aut Identification of shared risk loci and pathways for bipolar disorder and schizophrenia. 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Bipolar disorder (BD) is a highly heritable neuropsychiatric disease characterized by recurrent episodes of mania and depression. BD shows substantial clinical and genetic overlap with other psychiatric disorders, in particular schizophrenia (SCZ). The genes underlying this etiological overlap remain largely unknown. A recent SCZ genome wide association study (GWAS) by the Psychiatric Genomics Consortium identified 128 independent genome-wide significant single nucleotide polymorphisms (SNPs). The present study investigated whether these SCZ-associated SNPs also contribute to BD development through the performance of association testing in a large BD GWAS dataset (9747 patients, 14278 controls). After re-imputation and correction for sample overlap, 22 of 107 investigated SCZ SNPs showed nominal association with BD. The number of shared SCZ-BD SNPs was significantly higher than expected (p = 1.46x10-8). This provides further evidence that SCZ-associated loci contribute to the development of BD. Two SNPs remained significant after Bonferroni correction. The most strongly associated SNP was located near TRANK1, which is a reported genome-wide significant risk gene for BD. Pathway analyses for all shared SCZ-BD SNPs revealed 25 nominally enriched gene-sets, which showed partial overlap in terms of the underlying genes. The enriched gene-sets included calcium- and glutamate signaling, neuropathic pain signaling in dorsal horn neurons, and calmodulin binding. The present data provide further insights into shared risk loci and disease-associated pathways for BD and SCZ. This may suggest new research directions for the treatment and prevention of these two major psychiatric disorders. Medicine R Science Q Julian Hecker verfasserin aut Andrea Hofmann verfasserin aut Anna Maaser verfasserin aut Céline S Reinbold verfasserin aut Thomas W Mühleisen verfasserin aut Markus Leber verfasserin aut Jana Strohmaier verfasserin aut Franziska Degenhardt verfasserin aut Jens Treutlein verfasserin aut Manuel Mattheisen verfasserin aut Johannes Schumacher verfasserin aut Fabian Streit verfasserin aut Sandra Meier verfasserin aut Stefan Herms verfasserin aut Per Hoffmann verfasserin aut André Lacour verfasserin aut Stephanie H Witt verfasserin aut Andreas Reif verfasserin aut Bertram Müller-Myhsok verfasserin aut Susanne Lucae verfasserin aut Wolfgang Maier verfasserin aut Markus Schwarz verfasserin aut Helmut Vedder verfasserin aut Jutta Kammerer-Ciernioch verfasserin aut Andrea Pfennig verfasserin aut Michael Bauer verfasserin aut Martin Hautzinger verfasserin aut Susanne Moebus verfasserin aut Lorena M Schenk verfasserin aut Sascha B Fischer verfasserin aut Sugirthan Sivalingam verfasserin aut Piotr M Czerski verfasserin aut Joanna Hauser verfasserin aut Jolanta Lissowska verfasserin aut Neonila Szeszenia-Dabrowska verfasserin aut Paul Brennan verfasserin aut James D McKay verfasserin aut Adam Wright verfasserin aut Philip B Mitchell verfasserin aut Janice M Fullerton verfasserin aut Peter R Schofield verfasserin aut Grant W Montgomery verfasserin aut Sarah E Medland verfasserin aut Scott D Gordon verfasserin aut Nicholas G Martin verfasserin aut Valery Krasnov verfasserin aut Alexander Chuchalin verfasserin aut Gulja Babadjanova verfasserin aut Galina Pantelejeva verfasserin aut Lilia I Abramova verfasserin aut Alexander S Tiganov verfasserin aut Alexey Polonikov verfasserin aut Elza Khusnutdinova verfasserin aut Martin Alda verfasserin aut Cristiana Cruceanu verfasserin aut Guy A Rouleau verfasserin aut Gustavo Turecki verfasserin aut Catherine Laprise verfasserin aut Fabio Rivas verfasserin aut Fermin Mayoral verfasserin aut Manolis Kogevinas verfasserin aut Maria Grigoroiu-Serbanescu verfasserin aut Tim Becker verfasserin aut Thomas G Schulze verfasserin aut Marcella Rietschel verfasserin aut Sven Cichon verfasserin aut Heide Fier verfasserin aut Markus M Nöthen verfasserin aut In PLoS ONE Public Library of Science (PLoS), 2007 12(2017), 2, p e0171595 (DE-627)523574592 (DE-600)2267670-3 19326203 nnns volume:12 year:2017 number:2, p e0171595 https://doi.org/10.1371/journal.pone.0171595 kostenfrei https://doaj.org/article/fefac7becf554988a67a692f7dcea992 kostenfrei http://europepmc.org/articles/PMC5293228?pdf=render kostenfrei https://doaj.org/toc/1932-6203 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_34 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_235 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 12 2017 2, p e0171595 |
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Andreas J Forstner @@aut@@ Julian Hecker @@aut@@ Andrea Hofmann @@aut@@ Anna Maaser @@aut@@ Céline S Reinbold @@aut@@ Thomas W Mühleisen @@aut@@ Markus Leber @@aut@@ Jana Strohmaier @@aut@@ Franziska Degenhardt @@aut@@ Jens Treutlein @@aut@@ Manuel Mattheisen @@aut@@ Johannes Schumacher @@aut@@ Fabian Streit @@aut@@ Sandra Meier @@aut@@ Stefan Herms @@aut@@ Per Hoffmann @@aut@@ André Lacour @@aut@@ Stephanie H Witt @@aut@@ Andreas Reif @@aut@@ Bertram Müller-Myhsok @@aut@@ Susanne Lucae @@aut@@ Wolfgang Maier @@aut@@ Markus Schwarz @@aut@@ Helmut Vedder @@aut@@ Jutta Kammerer-Ciernioch @@aut@@ Andrea Pfennig @@aut@@ Michael Bauer @@aut@@ Martin Hautzinger @@aut@@ Susanne Moebus @@aut@@ Lorena M Schenk @@aut@@ Sascha B Fischer @@aut@@ Sugirthan Sivalingam @@aut@@ Piotr M Czerski @@aut@@ Joanna Hauser @@aut@@ Jolanta Lissowska @@aut@@ Neonila Szeszenia-Dabrowska @@aut@@ Paul Brennan @@aut@@ James D McKay @@aut@@ Adam Wright @@aut@@ Philip B Mitchell @@aut@@ Janice M Fullerton @@aut@@ Peter R Schofield @@aut@@ Grant W Montgomery @@aut@@ Sarah E Medland @@aut@@ Scott D Gordon @@aut@@ Nicholas G Martin @@aut@@ Valery Krasnov @@aut@@ Alexander Chuchalin @@aut@@ Gulja Babadjanova @@aut@@ Galina Pantelejeva @@aut@@ Lilia I Abramova @@aut@@ Alexander S Tiganov @@aut@@ Alexey Polonikov @@aut@@ Elza Khusnutdinova @@aut@@ Martin Alda @@aut@@ Cristiana Cruceanu @@aut@@ Guy A Rouleau @@aut@@ Gustavo Turecki @@aut@@ Catherine Laprise @@aut@@ Fabio Rivas @@aut@@ Fermin Mayoral @@aut@@ Manolis Kogevinas @@aut@@ Maria Grigoroiu-Serbanescu @@aut@@ Tim Becker @@aut@@ Thomas G Schulze @@aut@@ Marcella Rietschel @@aut@@ Sven Cichon @@aut@@ Heide Fier @@aut@@ Markus M Nöthen @@aut@@ |
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<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">DOAJ036492051</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230307231605.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">230227s2017 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1371/journal.pone.0171595</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)DOAJ036492051</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-599)DOAJfefac7becf554988a67a692f7dcea992</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="100" ind1="0" ind2=" "><subfield code="a">Andreas J Forstner</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Identification of shared risk loci and pathways for bipolar disorder and schizophrenia.</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2017</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Bipolar disorder (BD) is a highly heritable neuropsychiatric disease characterized by recurrent episodes of mania and depression. BD shows substantial clinical and genetic overlap with other psychiatric disorders, in particular schizophrenia (SCZ). The genes underlying this etiological overlap remain largely unknown. A recent SCZ genome wide association study (GWAS) by the Psychiatric Genomics Consortium identified 128 independent genome-wide significant single nucleotide polymorphisms (SNPs). The present study investigated whether these SCZ-associated SNPs also contribute to BD development through the performance of association testing in a large BD GWAS dataset (9747 patients, 14278 controls). After re-imputation and correction for sample overlap, 22 of 107 investigated SCZ SNPs showed nominal association with BD. The number of shared SCZ-BD SNPs was significantly higher than expected (p = 1.46x10-8). This provides further evidence that SCZ-associated loci contribute to the development of BD. Two SNPs remained significant after Bonferroni correction. The most strongly associated SNP was located near TRANK1, which is a reported genome-wide significant risk gene for BD. Pathway analyses for all shared SCZ-BD SNPs revealed 25 nominally enriched gene-sets, which showed partial overlap in terms of the underlying genes. The enriched gene-sets included calcium- and glutamate signaling, neuropathic pain signaling in dorsal horn neurons, and calmodulin binding. The present data provide further insights into shared risk loci and disease-associated pathways for BD and SCZ. 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identification of shared risk loci and pathways for bipolar disorder and schizophrenia |
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Identification of shared risk loci and pathways for bipolar disorder and schizophrenia. |
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Bipolar disorder (BD) is a highly heritable neuropsychiatric disease characterized by recurrent episodes of mania and depression. BD shows substantial clinical and genetic overlap with other psychiatric disorders, in particular schizophrenia (SCZ). The genes underlying this etiological overlap remain largely unknown. A recent SCZ genome wide association study (GWAS) by the Psychiatric Genomics Consortium identified 128 independent genome-wide significant single nucleotide polymorphisms (SNPs). The present study investigated whether these SCZ-associated SNPs also contribute to BD development through the performance of association testing in a large BD GWAS dataset (9747 patients, 14278 controls). After re-imputation and correction for sample overlap, 22 of 107 investigated SCZ SNPs showed nominal association with BD. The number of shared SCZ-BD SNPs was significantly higher than expected (p = 1.46x10-8). This provides further evidence that SCZ-associated loci contribute to the development of BD. Two SNPs remained significant after Bonferroni correction. The most strongly associated SNP was located near TRANK1, which is a reported genome-wide significant risk gene for BD. Pathway analyses for all shared SCZ-BD SNPs revealed 25 nominally enriched gene-sets, which showed partial overlap in terms of the underlying genes. The enriched gene-sets included calcium- and glutamate signaling, neuropathic pain signaling in dorsal horn neurons, and calmodulin binding. The present data provide further insights into shared risk loci and disease-associated pathways for BD and SCZ. This may suggest new research directions for the treatment and prevention of these two major psychiatric disorders. |
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Bipolar disorder (BD) is a highly heritable neuropsychiatric disease characterized by recurrent episodes of mania and depression. BD shows substantial clinical and genetic overlap with other psychiatric disorders, in particular schizophrenia (SCZ). The genes underlying this etiological overlap remain largely unknown. A recent SCZ genome wide association study (GWAS) by the Psychiatric Genomics Consortium identified 128 independent genome-wide significant single nucleotide polymorphisms (SNPs). The present study investigated whether these SCZ-associated SNPs also contribute to BD development through the performance of association testing in a large BD GWAS dataset (9747 patients, 14278 controls). After re-imputation and correction for sample overlap, 22 of 107 investigated SCZ SNPs showed nominal association with BD. The number of shared SCZ-BD SNPs was significantly higher than expected (p = 1.46x10-8). This provides further evidence that SCZ-associated loci contribute to the development of BD. Two SNPs remained significant after Bonferroni correction. The most strongly associated SNP was located near TRANK1, which is a reported genome-wide significant risk gene for BD. Pathway analyses for all shared SCZ-BD SNPs revealed 25 nominally enriched gene-sets, which showed partial overlap in terms of the underlying genes. The enriched gene-sets included calcium- and glutamate signaling, neuropathic pain signaling in dorsal horn neurons, and calmodulin binding. The present data provide further insights into shared risk loci and disease-associated pathways for BD and SCZ. This may suggest new research directions for the treatment and prevention of these two major psychiatric disorders. |
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Bipolar disorder (BD) is a highly heritable neuropsychiatric disease characterized by recurrent episodes of mania and depression. BD shows substantial clinical and genetic overlap with other psychiatric disorders, in particular schizophrenia (SCZ). The genes underlying this etiological overlap remain largely unknown. A recent SCZ genome wide association study (GWAS) by the Psychiatric Genomics Consortium identified 128 independent genome-wide significant single nucleotide polymorphisms (SNPs). The present study investigated whether these SCZ-associated SNPs also contribute to BD development through the performance of association testing in a large BD GWAS dataset (9747 patients, 14278 controls). After re-imputation and correction for sample overlap, 22 of 107 investigated SCZ SNPs showed nominal association with BD. The number of shared SCZ-BD SNPs was significantly higher than expected (p = 1.46x10-8). This provides further evidence that SCZ-associated loci contribute to the development of BD. Two SNPs remained significant after Bonferroni correction. The most strongly associated SNP was located near TRANK1, which is a reported genome-wide significant risk gene for BD. Pathway analyses for all shared SCZ-BD SNPs revealed 25 nominally enriched gene-sets, which showed partial overlap in terms of the underlying genes. The enriched gene-sets included calcium- and glutamate signaling, neuropathic pain signaling in dorsal horn neurons, and calmodulin binding. The present data provide further insights into shared risk loci and disease-associated pathways for BD and SCZ. This may suggest new research directions for the treatment and prevention of these two major psychiatric disorders. |
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