2026-08-29T13:36:36Zhttps://repisalud.isciii.es/rest/oai/request

oai:repisalud.isciii.es:20.500.12105/182332024-09-21T20:16:54Zcom_20.500.12105_15322com_20.500.12105_2051col_20.500.12105_16927

00925njm 22002777a 4500 dc Guzman-Parra, Jose author Streit, Fabian author Forstner, Andreas J author Strohmaier, Jana author González, Maria José author Gil Flores, Susana author Cabaleiro Fabeiro, Francisco J author Del Río Noriega, Francisco author Perez Perez, Fermin author Haro González, Jesus author Orozco Diaz, Guillermo author de Diego-Otero, Yolanda author Moreno-Kustner, Berta author Auburger, Georg author Degenhardt, Franziska author Heilmann-Heimbach, Stefanie author Herms, Stefan author Hoffmann, Per author Frank, Josef author Foo, Jerome C author Sirignano, Lea author Witt, Stephanie H author Cichon, Sven author Rivas, Fabio author Mayoral, Fermín author Nöthen, Markus M author Andlauer, Till F M author Rietschel, Marcella author 2021-01-11 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. 10.1038/s41398-020-01146-0 2158-3188 Translational psychiatry http://hdl.handle.net/10668/16959 33431802 http://hdl.handle.net/20.500.12105/18233 Clinical and genetic differences between bipolar disorder type 1 and 2 in multiplex families.