RT Journal Article
T1 Identification of shared risk loci and pathways for bipolar disorder and schizophrenia.
A1 Forstner, Andreas J
A1 Hecker, Julian
A1 Hofmann, Andrea
A1 Maaser, Anna
A1 Reinbold, Celine S
A1 Muhleisen, Thomas W
A1 Leber, Markus
A1 Strohmaier, Jana
A1 Degenhardt, Franziska
A1 Treutlein, Jens
A1 Mattheisen, Manuel
A1 Schumacher, Johannes
A1 Streit, Fabian
A1 Meier, Sandra
A1 Herms, Stefan
A1 Hoffmann, Per
A1 Lacour, Andre
A1 Witt, Stephanie H
A1 Reif, Andreas
A1 Muller-Myhsok, Bertram
A1 Lucae, Susanne
A1 Maier, Wolfgang
A1 Schwarz, Markus
A1 Vedder, Helmut
A1 Kammerer-Ciernioch, Jutta
A1 Pfennig, Andrea
A1 Bauer, Michael
A1 Hautzinger, Martin
A1 Moebus, Susanne
A1 Schenk, Lorena M
A1 Fischer, Sascha B
A1 Sivalingam, Sugirthan
A1 Czerski, Piotr M
A1 Hauser, Joanna
A1 Lissowska, Jolanta
A1 Szeszenia-Dabrowska, Neonila
A1 Brennan, Paul
A1 McKay, James D
A1 Wright, Adam
A1 Mitchell, Philip B
A1 Fullerton, Janice M
A1 Schofield, Peter R
A1 Montgomery, Grant W
A1 Medland, Sarah E
A1 Gordon, Scott D
A1 Martin, Nicholas G
A1 Krasnov, Valery
A1 Chuchalin, Alexander
A1 Babadjanova, Gulja
A1 Pantelejeva, Galina
A1 Abramova, Lilia I
A1 Tiganov, Alexander S
A1 Polonikov, Alexey
A1 Khusnutdinova, Elza
A1 Alda, Martin
A1 Cruceanu, Cristiana
A1 Rouleau, Guy A
A1 Turecki, Gustavo
A1 Laprise, Catherine
A1 Rivas, Fabio
A1 Mayoral, Fermin
A1 Kogevinas, Manolis
A1 Grigoroiu-Serbanescu, Maria
A1 Becker, Tim
A1 Schulze, Thomas G
A1 Rietschel, Marcella
A1 Cichon, Sven
A1 Fier, Heide
A1 Nöthen, Markus M
K1 Bipolar Disorder
K1 Genetic Linkage
K1 Genetic Predisposition to Disease
K1 Genome-Wide Association Study
AB 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.
PB Public Library of Science
YR 2017
FD 2017-02-06
LK http://hdl.handle.net/10668/10847
UL http://hdl.handle.net/10668/10847
LA en
NO Forstner AJ, Hecker J, Hofmann A, Maaser A, Reinbold CS, Mühleisen TW, et al.  Identification of shared risk loci and pathways for bipolar disorder and schizophrenia. PLoS One. 2017 Feb 6;12(2):e0171595
DS RISalud
RD Apr 13, 2025