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  • 1. Hagg, S.
    et al.
    Zhan, Y.
    Karlsson, R.
    Gerritsen, L.
    Ploner, A.
    van der Lee, S. J.
    Broer, L.
    Deelen, J.
    Marioni, R. E.
    Wong, A.
    Lundquist, Anders
    Umeå universitet, Samhällsvetenskapliga fakulteten, Handelshögskolan vid Umeå universitet, Statistik.
    Zhu, G.
    Hansell, N. K.
    Sillanpaa, E.
    Fedko, I. O.
    Amin, N. A.
    Beekman, M.
    de Craen, A. J. M.
    Degerman, Sofie
    Umeå universitet, Medicinska fakulteten, Institutionen för medicinsk biovetenskap, Patologi.
    Harris, S. E.
    Kan, K-J
    Martin-Ruiz, C. M.
    Montgomery, G. W.
    Adolfsson, Annelie N.
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Reynolds, C. A.
    Samani, N. J.
    Suchiman, H. E. D.
    Viljanen, A.
    von Zglinicki, T.
    Wright, M. J.
    Hottenga, J-J
    Boomsma, D. I.
    Rantanen, T.
    Kaprio, J. A.
    Nyholt, D. R.
    Martin, N. G.
    Nyberg, Lars
    Umeå universitet, Medicinska fakulteten, Institutionen för strålningsvetenskaper. Umeå universitet, Medicinska fakulteten, Institutionen för integrativ medicinsk biologi (IMB). Umeå universitet, Medicinska fakulteten, Umeå centrum för funktionell hjärnavbildning (UFBI).
    Adolfsson, Rolf
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Kuh, D.
    Starr, J. M.
    Deary, I. J.
    Slagboom, P. E.
    van Duijn, C. M.
    Codd, V.
    Pedersen, N. L.
    Short telomere length is associated with impaired cognitive performance in European ancestry cohorts2017Ingår i: Translational Psychiatry, ISSN 2158-3188, E-ISSN 2158-3188, Vol. 7, artikel-id e1100Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The association between telomere length (TL) dynamics on cognitive performance over the life-course is not well understood. This study meta-analyses observational and causal associations between TL and six cognitive traits, with stratifications on APOE genotype, in a Mendelian Randomization (MR) framework. Twelve European cohorts (N = 17 052; mean age = 59.2 +/- 8.8 years) provided results for associations between qPCR-measuredTL (T/S-ratio scale) and general cognitive function, mini-mental state exam (MMSE), processing speed by digit symbol substitution test (DSST), visuospatial functioning, memory and executive functioning (STROOP). In addition, a genetic risk score (GRS) for TL including seven known genetic variants for TL was calculated, and used in associations with cognitive traits as outcomes in all cohorts. Observational analyses showed that longer telomeres were associated with better scores on DSST (beta = 0.051 per s. d.-increase of TL; 95% confidence interval (CI): 0.024, 0.077; P = 0.0002), and MMSE (beta = 0.025; 95% CI: 0.002, 0.047; P = 0.03), and faster STROOP (beta = -0.053; 95% CI: -0.087, -0.018; P = 0.003). Effects for DSST were stronger in APOE epsilon 4 non-carriers (beta = 0.081; 95% CI: 0.045, 0.117; P = 1.0 x 10(-5)), whereas carriers performed better in STROOP (beta = -0.074; 95% CI: -0.140, -0.009; P = 0.03). Causal associations were found for STROOP only (beta = -0.598 per s. d.-increase of TL; 95% CI: -1.125, -0.072; P = 0.026), with a larger effect in epsilon 4-carriers (beta = -0.699; 95% CI: -1.330, -0.069; P = 0.03). Two-sample replication analyses using CHARGE summary statistics showed causal effects between TL and general cognitive function and DSST, but not with STROOP. In conclusion, we suggest causal effects from longer TL on better cognitive performance, where APOE epsilon 4-carriers might be at differential risk.

  • 2.
    Henje Blom, Eva
    et al.
    Karolinska Institutet, University of California San Francsisco.
    Han, L K M
    Connolly, C G
    Ho, T C
    Lin, J
    LeWinn, K Z
    Simmons, A N
    Sacchet, M D
    Mobayed, N
    Luna, M E
    Paulus, M
    Epel, E S
    Blackburn, E H
    Wolkowitz, O M
    Yang, T T
    Peripheral telomere length and hippocampal volume in adolescents with major depressive disorder.2015Ingår i: Translational Psychiatry, ISSN 2158-3188, E-ISSN 2158-3188, Vol. 5, artikel-id e676Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Several studies have reported that adults with major depressive disorder have shorter telomere length and reduced hippocampal volumes. Moreover, studies of adult populations without major depressive disorder suggest a relationship between peripheral telomere length and hippocampal volume. However, the relationship of these findings in adolescents with major depressive disorder has yet to be explored. We examined whether adolescent major depressive disorder is associated with altered peripheral telomere length and hippocampal volume, and whether these measures relate to one another. In 54 unmedicated adolescents (13-18 years) with major depressive disorder and 63 well-matched healthy controls, telomere length was assessed from saliva using quantitative polymerase chain reaction methods, and bilateral hippocampal volumes were measured with magnetic resonance imaging. After adjusting for age and sex (and total brain volume in the hippocampal analysis), adolescents with major depressive disorder exhibited significantly shorter telomere length and significantly smaller right, but not left hippocampal volume. When corrected for age, sex, diagnostic group and total brain volume, telomere length was not significantly associated with left or right hippocampal volume, suggesting that these cellular and neural processes may be mechanistically distinct during adolescence. Our findings suggest that shortening of telomere length and reduction of hippocampal volume are already present in early-onset major depressive disorder and thus unlikely to be only a result of accumulated years of exposure to major depressive disorder.

  • 3. Isung, J
    et al.
    Aeinehband, S
    Mobarrez, F
    Mårtensson, B
    Nordström, P
    Asberg, M
    Piehl, F
    Jokinen, Jussi
    Department of Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden.
    Low vascular endothelial growth factor and interleukin-8 in cerebrospinal fluid of suicide attempters2012Ingår i: Translational Psychiatry, ISSN 2158-3188, E-ISSN 2158-3188, Vol. 2, s. e196-Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    A dysregulated immune system influencing pathways for cytokine regulation and growth factor expression is implicated in the pathophysiology of several neuropsychiatric disorders. Here, we analyzed cerebrospinal fluid (CSF) cytokines and growth factors with an ultra-sensitive immunoassay system in 43 medication-free suicide attempters and 20 healthy male volunteers. CSF vascular endothelial growth factor (VEGF) and CSF interleukin-8 (IL-8) levels were significantly lower in suicide attempters compared with healthy controls. Further, CSF VEGF showed a significant negative correlation with depression severity. CSF IL-6 levels did not differ between suicide attempters and healthy controls. Low CSF levels of VEGF may represent a lack of trophic support to neurons and downregulation of neurogenesis in the hippocampus reflecting more severe depressive states. IL-8 has also been reported as important in neuroprotection as well as having chemokine activity in the innate immune response. The results support a role for an impaired innate immunity and dysregulation of neuroprotection in the pathophysiology of depression and suicidal behavior.

  • 4. Isung, J
    et al.
    Aeinehband, S
    Mobarrez, F
    Nordström, P
    Runeson, B
    Asberg, M
    Piehl, F
    Jokinen, Jussi
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri. Department of Clinical Neuroscience/Psychiatry, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.
    High interleukin-6 and impulsivity: determining the role of endophenotypes in attempted suicide2014Ingår i: Translational Psychiatry, ISSN 2158-3188, E-ISSN 2158-3188, Vol. 4, nr e470Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The dysregulation of inflammation has been associated with depression and, more recently, with suicidal behaviors. The reports regarding the relationship between interleukin-6 (IL-6) and suicide attempts are inconsistent. Personality traits such as impulsivity and aggression are considered endophenotypes and important factors that underlie suicidal behaviors. The aim of the current study was to assess whether plasma and cerebrospinal fluid (CSF) levels of IL-6 are associated with personality traits among suicide attempters. We assessed the relationships among personality traits, IL-6 and violent suicide attempts. The plasma and CSF levels of IL-6 were measured in suicide attempters (plasma=58, CSF=39) using antibody-based immunoassay systems. Personality domains were assessed using the Karolinska Scale of Personality (KSP). IL-6 levels in plasma and CSF were used to predict personality domains via regression models. Plasma IL-6 was significantly and positively correlated with extraversion as well as the KSP subscales impulsivity and monotony avoidance. CSF IL-6 was positively correlated with monotony avoidance. Violent suicide attempts tended to be associated with high plasma IL-6 levels. Plasma and CSF levels of IL-6 were not significantly associated with each other. These results indicate that impulsivity and the choice of a violent suicide attempt method might be related to higher levels of IL-6 in individuals who attempt suicide. The neuroinflammation hypothesis of suicidal behavior on the basis of elevated IL-6 levels might be partly explained by the positive association between IL-6 and impulsivity, which is a key element of the suicidal phenotype.

  • 5. Lindner, P.
    et al.
    Savic, I.
    Sitnikov, R.
    Budhiraja, M.
    Liu, Y.
    Jokinen, Jussi
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden; Centre for Psychiatry Research, Karolinska Institutet, Stockholm, Sweden.
    Tiihonen, J.
    Hodgins, S.
    Conduct disorder in females is associated with reduced corpus callosum structural integrity independent of comorbid disorders and exposure to maltreatment2016Ingår i: Translational Psychiatry, ISSN 2158-3188, E-ISSN 2158-3188, Vol. 6, artikel-id e714Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The behavioral phenotype and genotype of conduct disorder (CD) differ in males and females. Abnormalities of white matter integrity have been reported among males with CD and antisocial personality disorder (ASPD). Little is known about white matter integrity in females with CD. The present study aimed to determine whether abnormalities of white matter are present among young women who presented CD before the age of 15, and whether abnormalities are independent of the multiple comorbid disorders and experiences of maltreatment characterizing females with CD that may each in themselves be associated with alterations of the white matter. Three groups of women, aged on average 24 years, were scanned using diffusion tensor imaging and compared: 28 with prior CD, three of whom presented ASPD; a clinical comparison (CC) group of 15 women with no history of CD but with similar proportions who presented alcohol dependence, drug dependence, anxiety disorders, depression disorders and physical and sexual abuse as the CD group; and 24 healthy women. Whole-brain, tract-based spatial statistics were computed to investigate differences in fractional anisotropy, axial diffusivity and radial diffusivity. Compared with healthy women, women with prior CD showed widespread reductions in axial diffusivity primarily in frontotemporal regions. After statistically adjusting for comorbid disorders and maltreatment, group differences in the corpus callosum body and genu (including forceps minor) remained significant. Compared with the CC group, women with CD showed reduced fractional anisotropy in the body and genu of the corpus callosum. No differences were detected between the CD and healthy women in the uncinate fasciculus.

  • 6.
    Månsson, Kristoffer NT
    et al.
    Linköping University.
    Frick, Andreas
    Uppsala University.
    Boraxbekk, Carl-Johan
    Umeå universitet, Medicinska fakulteten, Umeå centrum för funktionell hjärnavbildning (UFBI). Umeå universitet, Samhällsvetenskapliga fakulteten, Centrum för befolkningsstudier (CBS).
    Marquand, AF
    Donders Institute, Radboud University.
    Williams, SCR
    King's College London.
    Carlbring, Per
    Stockholm University.
    Andersson, Gerhard
    Linköping University.
    Furmark, Tomas
    Uppsala University.
    Predicting long-term outcome of Internet-delivered cognitive behavior therapy for social anxiety disorder using fMRI and support vector machine learning2015Ingår i: Translational Psychiatry, ISSN 2158-3188, E-ISSN 2158-3188, Vol. 5, artikel-id e530Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Cognitive behavior therapy (CBT) is an effective treatment for social anxiety disorder (SAD), but many patients do not respond sufficiently and a substantial proportion relapse after treatment has ended. Predicting an individual's long-term clinical response therefore remains an important challenge. This study aimed at assessing neural predictors of long-term treatment outcome in participants with SAD 1 year after completion of Internet-delivered CBT (iCBT). Twenty-six participants diagnosed with SAD underwent iCBT including attention bias modification for a total of 13 weeks. Support vector machines (SVMs), a supervised pattern recognition method allowing predictions at the individual level, were trained to separate long-term treatment responders from nonresponders based on blood oxygen level-dependent (BOLD) responses to self-referential criticism. The Clinical Global Impression-Improvement scale was the main instrument to determine treatment response at the 1-year follow-up. Results showed that the proportion of long-term responders was 52% (12/23). From multivariate BOLD responses in the dorsal anterior cingulate cortex (dACC) together with the amygdala, we were able to predict long-term response rate of iCBT with an accuracy of 92% (confidence interval 95% 73.2–97.6). This activation pattern was, however, not predictive of improvement in the continuous Liebowitz Social Anxiety Scale—Self-report version. Follow-up psychophysiological interaction analyses revealed that lower dACC–amygdala coupling was associated with better long-term treatment response. Thus, BOLD response patterns in the fear-expressing dACC–amygdala regions were highly predictive of long-term treatment outcome of iCBT, and the initial coupling between these regions differentiated long-term responders from nonresponders. The SVM-neuroimaging approach could be of particular clinical value as it allows for accurate prediction of treatment outcome at the level of the individual.

  • 7. Månsson, Kristoffer
    et al.
    Salami, Alireza
    Umeå universitet, Medicinska fakulteten, Umeå centrum för funktionell hjärnavbildning (UFBI). Department of Neurobiology, Care Sciences and Society, Aging Research Center, Karolinska Institutet, Stockholm, Sweden.
    Frick, Andreas
    Carlbring, Per
    Andersson, Gerhard
    Furmark, Tomas
    Boraxbekk, Carl-Johan
    Umeå universitet, Samhällsvetenskapliga fakulteten, Enheten för demografi och åldrandeforskning (CEDAR). Umeå universitet, Medicinska fakulteten, Umeå centrum för funktionell hjärnavbildning (UFBI).
    Neuroplasticity in response to cognitive behavior therapy for social anxiety disorder2016Ingår i: Translational Psychiatry, ISSN 2158-3188, E-ISSN 2158-3188, Vol. 6, artikel-id e727Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Patients with anxiety disorders exhibit excessive neural reactivity in the amygdala, which can be normalized by effective treatment like cognitive behavior therapy (CBT). Mechanisms underlying the brain's adaptation to anxiolytic treatments are likely related both to structural plasticity and functional response alterations, but multimodal neuroimaging studies addressing structure-function interactions are currently missing. Here, we examined treatment-related changes in brain structure (gray matter (GM) volume) and function (blood-oxygen level dependent, BOLD response to self-referential criticism) in 26 participants with social anxiety disorder randomly assigned either to CBT or an attention bias modification control treatment. Also, 26 matched healthy controls were included. Significant time x treatment interactions were found in the amygdala with decreases both in GM volume (family-wise error (FWE) corrected P-FWE = 0.02) and BOLD responsivity (P-FWE = 0.01) after successful CBT. Before treatment, amygdala GM volume correlated positively with anticipatory speech anxiety (P-FWE = 0.04), and CBT-induced reduction of amygdala GM volume (pre-post) correlated positively with reduced anticipatory anxiety after treatment (P-FWE <= 0.05). In addition, we observed greater amygdala neural responsivity to self-referential criticism in socially anxious participants, as compared with controls (P-FWE = 0.029), before but not after CBT. Further analysis indicated that diminished amygdala GM volume mediated the relationship between decreased neural responsivity and reduced social anxiety after treatment (P = 0.007). Thus, our results suggest that improvement-related structural plasticity impacts neural responsiveness within the amygdala, which could be essential for achieving anxiety reduction with CBT.

  • 8. Porcheret, Kate
    et al.
    van Heugten-van der Kloet, Dalena
    Goodwin, Guy M.
    Foster, Russell G.
    Wulff, Katharina
    Umeå universitet, Medicinska fakulteten, Institutionen för strålningsvetenskaper. Umeå universitet, Medicinska fakulteten, Institutionen för molekylärbiologi (Medicinska fakulteten). Sleep and Circadian Neuroscience Institute, Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, UK.
    Holmes, Emily A.
    Investigation of the impact of total sleep deprivation at home on the number of intrusive memories to an analogue trauma2019Ingår i: Translational Psychiatry, ISSN 2158-3188, E-ISSN 2158-3188, Vol. 9, artikel-id 104Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Sleep enhances the consolidation of memory; however, this property of sleep may be detrimental in situations where memories of an event can lead to psychopathology, such as following a traumatic event. Intrusive memories of trauma are emotional memories that spring to mind involuntarily and are a core feature of post-traumatic stress disorder. Total sleep deprivation in a hospital setting on the first night after an analogue trauma (a trauma film) led to fewer intrusive memories compared to sleep as usual in one study. The current study aimed to test an extension of these findings: sleep deprivation under more naturalistic conditions-at home. Polysomnographic recordings show inconsistent sleep deprivation was achieved at home. Fewer intrusive memories were reported on day 1 after the trauma film in the sleep-deprived condition. On day 2 the opposite was found: more intrusive memories in the sleep-deprived condition. However, no significant differences were found with the removal of two participants with extreme values and no difference was found in the total number of intrusive memories reported in the week following the trauma film. Voluntary memory of the trauma film was found to be slightly impaired in the sleep deprivation condition. In conclusion, compared to our eariler findings using total sleep deprivation in a hospital setting, in the current study the use of inconsistent sleep deprivation at home does not replicate the pattern of results on reducing the number of intrusive memories. Considering the conditions under which sleep deprivation (naturalistic versus hospital) was achieved requires further examination.

  • 9. Szatkiewicz, Jin
    et al.
    Crowley, James J.
    Nordin Adolfsson, Annelie
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Åberg, Karolina A.
    Alaerts, Maaike
    Genovese, Giulio
    McCarroll, Steven
    Del-Favero, Jurgen
    Adolfsson, Rolf
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Sullivan, Patrick F.
    The genomics of major psychiatric disorders in a large pedigree from Northern Sweden2019Ingår i: Translational Psychiatry, ISSN 2158-3188, E-ISSN 2158-3188, Vol. 9, artikel-id 60Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    We searched for genetic causes of major psychiatric disorders (bipolar disorder, schizoaffective disorder, and schizophrenia) in a large, densely affected pedigree from Northern Sweden that originated with three pairs of founders born around 1650. We applied a systematic genomic approach to the pedigree via karyotyping (N = 9), genome-wide SNP arrays (N = 418), whole-exome sequencing (N = 26), and whole-genome sequencing (N = 10). Comprehensive analysis did not identify plausible variants of strong effect. Rather, pedigree cases had significantly higher genetic risk scores compared to pedigree and community controls.

  • 10. Witt, S. H.
    et al.
    Streit, F.
    Jungkunz, M.
    Frank, J.
    Awasthi, S.
    Reinbold, C. S.
    Treutlein, J.
    Degenhardt, F.
    Forstner, A. J.
    Heilmann-Heimbach, S.
    Dietl, L.
    Schwarze, C. E.
    Schendel, D.
    Strohmaier, J.
    Abdellaoui, A.
    Adolfsson, Rolf
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Air, T. M.
    Akil, H.
    Alda, M.
    Alliey-Rodriguez, N.
    Andreassen, O. A.
    Babadjanova, G.
    Bass, N. J.
    Bauer, M.
    Baune, B. T.
    Bellivier, F.
    Bergen, S.
    Bethell, A.
    Biernacka, J. M.
    Blackwood, D. H. R.
    Boks, M. P.
    Boomsma, D. I.
    Borglum, A. D.
    Borrmann-Hassenbach, M.
    Brennan, P.
    Budde, M.
    Buttenschon, H. N.
    Byrne, E. M.
    Cervantes, P.
    Clarke, T-K
    Craddock, N.
    Cruceanu, C.
    Curtis, D.
    Czerski, P. M.
    Dannlowski, U.
    Davis, T.
    de Geus, E. J. C.
    Di Florio, A.
    Djurovic, S.
    Domenici, E.
    Edenberg, H. J.
    Etain, B.
    Fischer, S. B.
    Forty, L.
    Fraser, C.
    Frye, M. A.
    Fullerton, J. M.
    Gade, K.
    Gershon, E. S.
    Giegling, I.
    Gordon, S. D.
    Gordon-Smith, K.
    Grabe, H. J.
    Green, E. K.
    Greenwood, T. A.
    Grigoroiu-Serbanescu, M.
    Guzman-Parra, J.
    Hall, L. S.
    Hamshere, M.
    Hauser, J.
    Hautzinger, M.
    Heilbronner, U.
    Herms, S.
    Hitturlingappa, S.
    Hoffmann, P.
    Holmans, P.
    Hottenga, J-J
    Jamain, S.
    Jones, I.
    Jones, L. A.
    Jureus, A.
    Kahn, R. S.
    Kammerer-Ciernioch, J.
    Kirov, G.
    Kittel-Schneider, S.
    Kloiber, S.
    Knott, S. V.
    Kogevinas, M.
    Landen, M.
    Leber, M.
    Leboyer, M.
    Li, Q. S.
    Lissowska, J.
    Lucae, S.
    Martin, N. G.
    Mayoral-Cleries, F.
    McElroy, S. L.
    McIntosh, A. M.
    McKay, J. D.
    McQuillin, A.
    Medland, S. E.
    Middeldorp, C. M.
    Milaneschi, Y.
    Mitchell, P. B.
    Montgomery, G. W.
    Morken, G.
    Mors, O.
    Muehleisen, T. W.
    Mueller-Myhsok, B.
    Myers, R. M.
    Nievergelt, C. M.
    Nurnberger, J. I.
    O'Donovan, M. C.
    Loohuis, L. M. O.
    Ophoff, R.
    Oruc, L.
    Owen, M. J.
    Paciga, S. A.
    Penninx, B. W. J. H.
    Perry, A.
    Pfennig, A.
    Potash, J. B.
    Preisig, M.
    Reif, A.
    Rivas, F.
    Rouleau, G. A.
    Schofield, P. R.
    Schulze, T. G.
    Schwarz, M.
    Scott, L.
    Sinnamon, G. C. B.
    Stahl, E. A.
    Strauss, J.
    Turecki, G.
    Van der Auwera, S.
    Vedder, H.
    Vincent, J. B.
    Willemsen, G.
    Witt, C. C.
    Wray, N. R.
    Xi, H. S.
    Tadic, A.
    Dahmen, N.
    Schott, B. H.
    Cichon, S.
    Noethen, M. M.
    Ripke, S.
    Mobascher, A.
    Rujescu, D.
    Lieb, K.
    Roepke, S.
    Schmahl, C.
    Bohus, M.
    Rietschel, M.
    Genome-wide association study of borderline personality disorder reveals genetic overlap with bipolar disorder, major depression and schizophrenia2017Ingår i: Translational Psychiatry, ISSN 2158-3188, E-ISSN 2158-3188, Vol. 7, artikel-id e1155Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Borderline personality disorder (BOR) is determined by environmental and genetic factors, and characterized by affective instability and impulsivity, diagnostic symptoms also observed in manic phases of bipolar disorder (BIP). Up to 20% of BIP patients show comorbidity with BOR. This report describes the first case–control genome-wide association study (GWAS) of BOR, performed in one of the largest BOR patient samples worldwide. The focus of our analysis was (i) to detect genes and gene sets involved in BOR and (ii) to investigate the genetic overlap with BIP. As there is considerable genetic overlap between BIP, major depression (MDD) and schizophrenia (SCZ) and a high comorbidity of BOR and MDD, we also analyzed the genetic overlap of BOR with SCZ and MDD. GWAS, gene-based tests and gene-set analyses were performed in 998 BOR patients and 1545 controls. Linkage disequilibrium score regression was used to detect the genetic overlap between BOR and these disorders. Single marker analysis revealed no significant association after correction for multiple testing. Gene-based analysis yielded two significant genes: DPYD (P=4.42 × 10−7) and PKP4 (P=8.67 × 10−7); and gene-set analysis yielded a significant finding for exocytosis (GO:0006887, PFDR=0.019; FDR, false discovery rate). Prior studies have implicated DPYD, PKP4 and exocytosis in BIP and SCZ. The most notable finding of the present study was the genetic overlap of BOR with BIP (rg=0.28 [P=2.99 × 10−3]), SCZ (rg=0.34 [P=4.37 × 10−5]) and MDD (rg=0.57 [P=1.04 × 10−3]). We believe our study is the first to demonstrate that BOR overlaps with BIP, MDD and SCZ on the genetic level. Whether this is confined to transdiagnostic clinical symptoms should be examined in future studies.

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