TY  - JOUR
A1  - Forstner, Andreas Josef
A1  - Hecker, Julian
A1  - Hofmann, Andrea
A1  - Maaser, Anna
A1  - Reinbold, Céline S.
A1  - Mühleisen, 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, André
A1  - Witt, Stephanie
A1  - Reif, Andreas
A1  - Müller-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 E.
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 Gordon
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, Fermı́n
A1  - Kogevinas, Manolis
A1  - Grigoroiu-Serbanescu, Maria
A1  - Becker, Tim
A1  - Schulze, Thomas Gerd
A1  - Rietschel, Marcella
A1  - Cichon, Sven
A1  - Fier, Heide
A1  - Nöthen, Markus Maria
T1  - Identification of shared risk loci and pathways for bipolar disorder and schizophrenia
T2  - PLoS one
N2  - 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.
Y1  - 2017
UR  - http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/42892
UR  - https://nbn-resolving.org/urn:nbn:de:hebis:30:3-428927
UR  - https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5293228
SN  - 1932-6203
N1  - Copyright: © 2017 Forstner et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
VL  - 12
IS  - (2): e0171595
SP  - 1
EP  - 14
PB  - PLoS
CY  - Lawrence, Kan.
ER  -