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@ARTICLE{GuzmanParra:893926,
author = {Guzman-Parra, Jose and Streit, Fabian and Forstner, Andreas
J. and Strohmaier, Jana and González, Maria José and Gil
Flores, Susana and Cabaleiro Fabeiro, Francisco J. and del
Río Noriega, Francisco and Perez Perez, Fermin and Haro
González, Jesus and Orozco Diaz, Guillermo and de
Diego-Otero, Yolanda and Moreno-Kustner, Berta and Auburger,
Georg and Degenhardt, Franziska and Heilmann-Heimbach,
Stefanie and Herms, Stefan and Hoffmann, Per and Frank,
Josef and Foo, Jerome C. and Sirignano, Lea and Witt,
Stephanie H. and Cichon, Sven and Rivas, Fabio and Mayoral,
Fermín and Nöthen, Markus M. and Andlauer, Till F. M. and
Rietschel, Marcella},
title = {{C}linical and genetic differences between bipolar disorder
type 1 and 2 in multiplex families},
journal = {Translational Psychiatry},
volume = {11},
number = {1},
issn = {2158-3188},
address = {London},
publisher = {Nature Publishing Group},
reportid = {FZJ-2021-02936},
pages = {31},
year = {2021},
abstract = {The two major subtypes of bipolar disorder (BD), BD-I and
BD-II, are distinguished based on the presence of manic or
hypomanic episodes. Historically, BD-II was perceived as a
less severe form of BD-I. Recent research has challenged
this concept of a severity continuum. Studies in large
samples of unrelated patients have described clinical and
genetic differences between the subtypes. Besides an
increased schizophrenia polygenic risk load in BD-I, these
studies also observed an increased depression risk load in
BD-II patients. The present study assessed whether such
clinical and genetic differences are also found in BD
patients from multiplex families, which exhibit reduced
genetic and environmental heterogeneity. Comparing 252 BD-I
and 75 BD-II patients from the Andalusian Bipolar Family
(ABiF) study, the clinical course, symptoms during
depressive and manic episodes, and psychiatric comorbidities
were analyzed. Furthermore, polygenic risk scores (PRS) for
BD, schizophrenia, and depression were assessed. BD-I
patients not only suffered from more severe symptoms during
manic episodes but also more frequently showed incapacity
during depressive episodes. A higher BD PRS was
significantly associated with suicidal ideation. Moreover,
BD-I cases exhibited lower depression PRS. In line with a
severity continuum from BD-II to BD-I, our results link BD-I
to a more pronounced clinical presentation in both mania and
depression and indicate that the polygenic risk load of BD
predisposes to more severe disorder characteristics.
Nevertheless, our results suggest that the genetic risk
burden for depression also shapes disorder presentation and
increases the likelihood of BD-II subtype development.},
cin = {INM-1},
ddc = {610},
cid = {I:(DE-Juel1)INM-1-20090406},
pnm = {5251 - Multilevel Brain Organization and Variability
(POF4-525)},
pid = {G:(DE-HGF)POF4-5251},
typ = {PUB:(DE-HGF)16},
pubmed = {33431802},
UT = {WOS:000609884900005},
doi = {10.1038/s41398-020-01146-0},
url = {https://juser.fz-juelich.de/record/893926},
}