Umeå University's logo

umu.sePublications
Change search
Refine search result
1 - 21 of 21
CiteExportLink to result list
Permanent link
Cite
Citation style
  • apa
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf
Rows per page
  • 5
  • 10
  • 20
  • 50
  • 100
  • 250
Sort
  • Standard (Relevance)
  • Author A-Ö
  • Author Ö-A
  • Title A-Ö
  • Title Ö-A
  • Publication type A-Ö
  • Publication type Ö-A
  • Issued (Oldest first)
  • Issued (Newest first)
  • Created (Oldest first)
  • Created (Newest first)
  • Last updated (Oldest first)
  • Last updated (Newest first)
  • Disputation date (earliest first)
  • Disputation date (latest first)
  • Standard (Relevance)
  • Author A-Ö
  • Author Ö-A
  • Title A-Ö
  • Title Ö-A
  • Publication type A-Ö
  • Publication type Ö-A
  • Issued (Oldest first)
  • Issued (Newest first)
  • Created (Oldest first)
  • Created (Newest first)
  • Last updated (Oldest first)
  • Last updated (Newest first)
  • Disputation date (earliest first)
  • Disputation date (latest first)
Select
The maximal number of hits you can export is 250. When you want to export more records please use the Create feeds function.
  • 1.
    Boström, Adrian Desai E.
    et al.
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Psychiatry. Centre for Psychiatry Research, Department of Clinical Neuroscience, Karolinska Institutet, and Stockholm Health Care Services, Region Stockholm, Karolinska University Hospital, Stockholm, Sweden.
    Andersson, Peter
    Department of Clinical Neuroscience/Psychology, Karolinska Institute, Stockholm, Sweden; Centre for Clinical Research Dalarna, Uppsala University, Falun, Sweden.
    Jamshidi, Esmail
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Psychiatry.
    Wilczek, Alexander
    Department of Clinical Sciences, Karolinska Institutet at Danderyd Hospital, Stockholm, Sweden.
    Nilsonne, Åsa
    Department of Clinical Sciences, Karolinska Institutet at Danderyd Hospital, Stockholm, Sweden.
    Rask-Andersen, Mathias
    Department of Immunology, Genetics and Pathology, Science for Life Laboratory, Uppsala University, Uppsala, Sweden.
    Åsberg, Marie
    Department of Clinical Sciences, Karolinska Institutet at Danderyd Hospital, Stockholm, Sweden.
    Jokinen, Jussi
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Psychiatry. Centre for Psychiatry Research, Department of Clinical Neuroscience, Karolinska Institutet, and Stockholm Health Care Services, Region Stockholm, Karolinska University Hospital, Stockholm, Sweden.
    Accelerated epigenetic aging in women with emotionally unstable personality disorder and a history of suicide attempts2023In: Translational Psychiatry, E-ISSN 2158-3188, Vol. 13, no 1, article id 66Article in journal (Refereed)
    Abstract [en]

    Emotional unstable personality disorder (EUPD; previously borderline personality disorder, BPD) is associated with excess natural-cause mortality, comorbid medical conditions, poor health habits and stress related epigenomic alterations. Previous studies demonstrated that GrimAge – a state-of-the-art epigenetic age (EA) estimator – strongly predicts mortality risk and physiological dysregulation. Herein, we utilize the GrimAge algorithm to investigate whether women with EUPD and a history of recent suicide attempts exhibit EA acceleration (EAA) in comparison to healthy controls. Genome-wide methylation patterns were measured using the Illumina Infinum Methylation Epic BeadChip in whole blood from 97 EUPD patients and 32 healthy controls. The control group was significantly older (p < 0.0001) and reported lesser exposure to violent behavior in both youth and adulthood (p < 0.0001). Groups were otherwise comparable regarding gender, BMI, or tobacco usage (p > 0.05). EA estimator DNAmGrimAge exceeded chronological age by 8.8 and 2.3 years in the EUPD and control group, respectively. Similarly, EAA marker AgeAccelGrim was substantially higher in EUPD subjects when compared to controls, in both univariate and multivariate analyzes (p < 0.00001). Tobacco usage conferred substantial within-group effects on the EA-chronological age difference, i.e., 10.74 years (SD = 4.19) compared to 6.00 years (SD = 3.10) in the non-user EUPD group (p < 0.00001). Notably, past alcohol and substance abuse, use of psychotropic medications, global assessment of functioning, self-reported exposure to violent behavior in youth and adulthood, later completed suicide (N = 8) and age at first suicide attempt did not predict EAA in the EUPD group (p > 0.05). These results underscore the importance of addressing medical health conditions along with low-cost preventative interventions aimed at improving somatic health outcomes in EUPD, such as efforts to support cessation of tobacco use. The independency of GrimAge to other EA algorithms in this group of severely impaired EUPD patients, suggest it may have unique characteristics to evaluate risk of adverse health outcomes in context of psychiatric disorders.

    Download full text (pdf)
    fulltext
  • 2.
    Cosgrave, Jan
    et al.
    Sleep and Circadian Neuroscience Institute, Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, United Kingdom; Department of Clinical, Educational and Health Psychology, University College London, London, United Kingdom.
    Purple, Ross J.
    Department of Physiology, Pharmacology and Neuroscience, University of Bristol, Biomedical Sciences Building, University Walk, Bristol, United Kingdom.
    Haines, Ross
    Department of Statistics, University of Oxford, South Parks Road, Oxford, United Kingdom.
    Porcheret, Kate
    Norwegian Centre for Violence & Traumatic Stress Studies, University of Oslo, Oslo, Norway.
    van Heugten-van der Kloet, Dalena
    Department of Clinical Psychological Science, Maastricht University, Maastricht University, Maastricht, Netherlands.
    Johns, Louise
    Department of Psychiatry, University of Oxford, Warneford Hospital, Oxford, United Kingdom; Oxford Health National Health Service (NHS) Foundation Trust, Oxford, United Kingdom.
    Alexander, Iona
    Sleep and Circadian Neuroscience Institute, Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, United Kingdom.
    Goodwin, Guy M.
    Department of Psychiatry, University of Oxford, Warneford Hospital, Oxford, United Kingdom; Oxford Health National Health Service (NHS) Foundation Trust, Oxford, United Kingdom.
    Foster, Russell G.
    Sleep and Circadian Neuroscience Institute, Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, United Kingdom.
    Wulff, Katharina
    Umeå University, Faculty of Medicine, Wallenberg Centre for Molecular Medicine at Umeå University (WCMM). Umeå University, Faculty of Science and Technology, Department of Molecular Biology (Faculty of Science and Technology). Umeå University, Faculty of Medicine, Department of Radiation Sciences, Diagnostic Radiology.
    Do environmental risk factors for the development of psychosis distribute differently across dimensionally assessed psychotic experiences?2021In: Translational Psychiatry, E-ISSN 2158-3188, Vol. 11, no 1, article id 226Article in journal (Refereed)
    Abstract [en]

    Psychotic experiences (PE) are associated with poorer functioning, higher distress and the onset of serious mental illness. Environmental exposures (e.g. childhood abuse) are associated with the development of PE. However, which specific exposures convey risk for each type or dimension of PE has rarely been explored. The Oxford Wellbeing Life and Sleep (OWLS) survey includes 22 environmental risk factors for psychosis and was designed to examine how environmental risks are associated with specific dimensions of PE. Multivariate logistic regression models were fit using these risk factors to predict six dimensions of PE (perceptual abnormalities, persecutory ideation, bizarre ideas, cognitive disorganisation, delusional mood and negative symptoms). Models were built using only 70% of the data, and then fit to the remaining data to assess their generalisability and quality. 1789 (27.2% men; mean age = 27.6; SD = 10.9) survey responses were analysed. The risk factors predictive of the most PE were anxiety, social withdrawal during childhood and trauma. Cannabis and depression predicted three dimensions with both predicting bizarre ideas and persecutory ideation. Psychological abuse and sleep quality each predicted two dimensions (persecutory ideation and delusional mood). Risk factors predicting one PE dimension were age (predicting cognitive disorganisation), physical abuse (bizarre ideas), bullying and gender (persecutory ideation); and circadian phase (delusional mood). These results lend support for a continuum of psychosis, suggesting environmental risks for psychotic disorders also increase the risk of assorted dimensions of PE. Furthermore, it advocates the use of dimensional approaches when examining environmental exposures for PE given that environmental risks distribute differently across dimensions.

    Download full text (pdf)
    fulltext
  • 3.
    Dubol, Manon
    et al.
    Department of Women’s and Children’s Health, Science for Life Laboratory, Uppsala University, Uppsala, Sweden.
    Stiernman, Louise
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Obstetrics and Gynecology.
    Wikström, Johan
    Department of Surgical Sciences, Radiology, Uppsala University, Uppsala, Sweden.
    Lanzenberger, Rupert
    Department of Psychiatry and Psychotherapy, Medical University of Vienna, Vienna, Austria.
    Neill Epperson, C.
    Department of Psychiatry, Department of Family Medicine, University of Colorado School of Medicine, Anschutz Medical Campus, CO, Aurora, United States.
    Sundström-Poromaa, Inger
    Department of Women’s and Children’s Health, Uppsala University, Uppsala, Sweden.
    Bixo, Marie
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Obstetrics and Gynecology.
    Comasco, Erika
    Department of Women’s and Children’s Health, Science for Life Laboratory, Uppsala University, Uppsala, Sweden.
    Differential grey matter structure in women with premenstrual dysphoric disorder: evidence from brain morphometry and data-driven classification2022In: Translational Psychiatry, E-ISSN 2158-3188, Vol. 12, no 1, article id 250Article in journal (Refereed)
    Abstract [en]

    Premenstrual dysphoric disorder (PMDD) is a female-specific condition classified in the Diagnostic and Statical Manual—5th edition under depressive disorders. Alterations in grey matter volume, cortical thickness and folding metrics have been associated with a number of mood disorders, though little is known regarding brain morphological alterations in PMDD. Here, women with PMDD and healthy controls underwent magnetic resonance imaging (MRI) during the luteal phase of the menstrual cycle. Differences in grey matter structure between the groups were investigated by use of voxel- and surface-based morphometry. Machine learning and multivariate pattern analysis were performed to test whether MRI data could distinguish women with PMDD from healthy controls. Compared to controls, women with PMDD had smaller grey matter volume in ventral posterior cortices and the cerebellum (Cohen’s d = 0.45–0.76). Region-of-interest analyses further indicated smaller volume in the right amygdala and putamen of women with PMDD (Cohen’s d = 0.34–0.55). Likewise, thinner cortex was observed in women with PMDD compared to controls, particularly in the left hemisphere (Cohen’s d = 0.20–0.74). Classification analyses showed that women with PMDD can be distinguished from controls based on grey matter morphology, with an accuracy up to 74%. In line with the hypothesis of an impaired top-down inhibitory circuit involving limbic structures in PMDD, the present findings point to PMDD-specific grey matter anatomy in regions of corticolimbic networks. Furthermore, the results include widespread cortical and cerebellar regions, suggesting the involvement of distinct networks in PMDD pathophysiology.

    Download full text (pdf)
    fulltext
  • 4.
    Farnsworth von Cederwald, Bryn
    et al.
    Umeå University, Faculty of Medicine, Umeå Centre for Functional Brain Imaging (UFBI). Umeå University, Faculty of Medicine, Department of Integrative Medical Biology (IMB).
    Johansson, Jarkko
    Umeå University, Faculty of Medicine, Umeå Centre for Functional Brain Imaging (UFBI). Umeå University, Faculty of Medicine, Department of Radiation Sciences, Diagnostic Radiology.
    Riklund, Katrine
    Umeå University, Faculty of Medicine, Umeå Centre for Functional Brain Imaging (UFBI). Umeå University, Faculty of Medicine, Department of Radiation Sciences, Diagnostic Radiology.
    Karalija, Nina
    Umeå University, Faculty of Medicine, Umeå Centre for Functional Brain Imaging (UFBI). Umeå University, Faculty of Medicine, Department of Integrative Medical Biology (IMB).
    Boraxbekk, Carl-Johan
    Umeå University, Faculty of Medicine, Umeå Centre for Functional Brain Imaging (UFBI). Umeå University, Faculty of Medicine, Department of Radiation Sciences, Diagnostic Radiology. Danish Research Center for Magnetic Resonance (DRCMR), Center for Functional and Diagnostic Imaging and Research, Copenhagen University Hospital, Amager and Hvidovre, Copenhagen, Denmark; Institute of Sports Medicine Copenhagen (ISMC) and Department of Neurology, Copenhagen University Hospital Bispebjerg, Copenhagen, Denmark; Institute for Clinical Medicine, Faculty of Medical and Health Sciences, University of Copenhagen, Copenhagen, Denmark.
    White matter lesion load determines exercise-induced dopaminergic plasticity and working memory gains in aging2023In: Translational Psychiatry, E-ISSN 2158-3188, Vol. 13, no 1, article id 28Article in journal (Refereed)
    Abstract [en]

    Age-related dopamine reductions have been suggested to contribute to maladaptive working memory (WM) function in older ages. One promising intervention approach is to increase physical activity, as this has been associated with plasticity of the striatal dopamine system and WM improvements, however with individual differences in efficacy. The present work focused on the impact of individual differences in white-matter lesion burden upon dopamine D2-like receptor (DRD2) availability and WM changes in response to a 6 months physical activity intervention. While the intervention altered striatal DRD2 availability and WM performance in individuals with no or only mild lesions (p < 0.05), no such effects were found in individuals with moderate-to-severe lesion severity (p > 0.05). Follow-up analyses revealed a similar pattern for processing speed, but not for episodic memory performance. Linear analyses further revealed that lesion volume (ml) at baseline was associated with reduced DRD2 availability (r = −0.41, p < 0.05), and level of DRD2 change (r = 0.40, p < 0.05). Taken together, this study underlines the necessity to consider cerebrovascular health in interventions with neurocognitive targets. Future work should assess whether these findings extend beyond measures of DRD2 availability and WM.

    Download full text (pdf)
    fulltext
  • 5. 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 University, Faculty of Social Sciences, Umeå School of Business and Economics (USBE), Statistics.
    Zhu, G.
    Hansell, N. K.
    Sillanpaa, E.
    Fedko, I. O.
    Amin, N. A.
    Beekman, M.
    de Craen, A. J. M.
    Degerman, Sofie
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Pathology.
    Harris, S. E.
    Kan, K-J
    Martin-Ruiz, C. M.
    Montgomery, G. W.
    Adolfsson, Annelie N.
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Psychiatry.
    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 University, Faculty of Medicine, Department of Radiation Sciences. Umeå University, Faculty of Medicine, Department of Integrative Medical Biology (IMB). Umeå University, Faculty of Medicine, Umeå Centre for Functional Brain Imaging (UFBI).
    Adolfsson, Rolf
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Psychiatry.
    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 cohorts2017In: Translational Psychiatry, E-ISSN 2158-3188, Vol. 7, article id e1100Article in journal (Refereed)
    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.

    Download full text (pdf)
    fulltext
  • 6.
    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.2015In: Translational Psychiatry, E-ISSN 2158-3188, Vol. 5, article id e676Article in journal (Refereed)
    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.

  • 7. 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 attempters2012In: Translational Psychiatry, E-ISSN 2158-3188, Vol. 2, p. e196-Article in journal (Refereed)
    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.

  • 8. Isung, J
    et al.
    Aeinehband, S
    Mobarrez, F
    Nordström, P
    Runeson, B
    Asberg, M
    Piehl, F
    Jokinen, Jussi
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Psychiatry. Department of Clinical Neuroscience/Psychiatry, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.
    High interleukin-6 and impulsivity: determining the role of endophenotypes in attempted suicide2014In: Translational Psychiatry, E-ISSN 2158-3188, Vol. 4, no e470Article in journal (Refereed)
    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.

    Download full text (pdf)
    fulltext
  • 9.
    Jokinen, Jussi
    et al.
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Psychiatry. Department of Clinical Neuroscience/Psychology, Karolinska Institute, Stockholm, Sweden.
    Andersson, Peter
    Department of Clinical Neuroscience/Psychology, Karolinska Institute, Stockholm, Sweden; Centre for Clinical Research Dalarna, Uppsala University, Falun, Sweden.
    Chatzittofis, Andreas
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Psychiatry. Medical School, University of Cyprus, Nicosia, Cyprus.
    Savard, Josephine
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Psychiatry.
    Rask-Andersen, Mathias
    Department of Immunology, Genetics and Pathology, Science for Life Laboratory, Uppsala University, Uppsala, Sweden.
    Åsberg, Marie
    Department of Clinical Neuroscience/Psychology, Karolinska Institute, Stockholm, Sweden.
    Boström, Adrian Desai E.
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Psychiatry. Department of Women’s and Children’s Health/Neuropediatrics, Karolinska Institutet, Stockholm, Sweden.
    Accelerated epigenetic aging in suicide attempters uninfluenced by high intent-to-die and choice of lethal methods2022In: Translational Psychiatry, E-ISSN 2158-3188, Vol. 12, no 1, article id 224Article in journal (Refereed)
    Abstract [en]

    Suicide attempts (SA) are associated with excess non-suicidal mortality, putatively mediated in part by premature cellular senescence. Epigenetic age (EA) estimators of biological age have been previously demonstrated to strongly predict physiological dysregulation and mortality risk. Herein, we investigate if violent SA with high intent-to-die is predictive of epigenetics-derived estimates of biological aging. The genome-wide methylation pattern was measured using the Illumina Infinium Methylation EPIC BeadChip in whole blood of 88 suicide attempters. Subjects were stratified into two groups based on the putative risk of later committed suicide (low- [n = 58] and high-risk [n = 30]) in dependency of SA method (violent or non-violent) and/or intent-to-die (high/low). Estimators of intrinsic and extrinsic EA acceleration, one marker optimized to predict physiological dysregulation (DNAmPhenoAge/AgeAccelPheno) and one optimized to predict lifespan (DNAmGrimAge/AgeAccelGrim) were investigated for associations to severity of SA, by univariate and multivariate analyses. The study was adequately powered to detect differences of 2.2 years in AgeAccelGrim in relation to SA severity. Baseline DNAmGrimAge exceeded chronological age by 7.3 years on average across all samples, conferring a mean 24.6% increase in relation to actual age. No individual EA acceleration marker was differentiated by suicidal risk group (p > 0.1). Thus, SA per se but not severity of SA is related to EA, implicating that excess non-suicidal mortality in SA is unrelated to risk of committed suicide. Preventative healthcare efforts aimed at curtailing excess mortality after SA may benefit from acting equally powerful to recognize somatic comorbidities irrespective of the severity inherent in the act itself.

    Download full text (pdf)
    fulltext
  • 10.
    Kauppi, Karolina
    et al.
    Umeå University, Faculty of Medicine, Department of Integrative Medical Biology (IMB). Department of Medical Epidemiology and Biostatistics, Karolinska Institutet,Stockholm, Sweden.
    Rönnlund, Michael
    Umeå University, Faculty of Social Sciences, Department of Psychology.
    Nordin Adolfsson, Annelie
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Psychiatry.
    Pudas, Sara
    Umeå University, Faculty of Medicine, Department of Integrative Medical Biology (IMB).
    Adolfsson, Rolf
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Psychiatry.
    Effects of polygenic risk for Alzheimer's disease on rate of cognitive decline in normal aging2020In: Translational Psychiatry, E-ISSN 2158-3188, Vol. 10, no 1, article id 250Article in journal (Refereed)
    Abstract [en]

    Most people's cognitive abilities decline with age, with significant and partly genetically driven, individual differences in rate of change. Although APOE 4 and genetic scores for late-onset Alzheimer's disease (LOAD) have been related to cognitive decline during preclinical stages of dementia, there is limited knowledge concerning genetic factors implied in normal cognitive aging. In the present study, we examined three potential genetic predictors of age-related cognitive decline as follows: (1) the APOE 4 allele, (2) a polygenic score for general cognitive ability (PGS-cog), and (3) a polygenic risk score for late-onset AD (PRS-LOAD). We examined up to six time points of cognitive measurements in the longitudinal population-based Betula study, covering a 25-year follow-up period. Only participants that remained alive and non-demented until the most recent dementia screening (1-3 years after the last test occasion) were included (n=1087). Individual differences in rate of cognitive change (composite score) were predicted by the PRS-LOAD and APOE 4, but not by PGS-cog. To control for the possibility that the results reflected a preclinical state of Alzheimer's disease in some participants, we re-ran the analyses excluding cognitive data from the last test occasion to model cognitive change up-until a minimum of 6 years before potential onset of clinical Alzheimers. Strikingly, the association of PRS-LOAD, but not APOE 4, with cognitive change remained. The results indicate that PRS-LOAD predicts individual difference in rate of cognitive decline in normal aging, but it remains to be determined to what extent this reflects preclinical Alzheimer's disease brain pathophysiology and subsequent risk to develop the disease.

    Download full text (pdf)
    fulltext
  • 11.
    Koch, Elise
    et al.
    Umeå University, Faculty of Medicine, Department of Integrative Medical Biology (IMB).
    Nyberg, Lars
    Umeå University, Faculty of Medicine, Department of Integrative Medical Biology (IMB). Umeå University, Faculty of Medicine, Department of Radiation Sciences, Diagnostic Radiology.
    Lundquist, Anders
    Umeå University, Faculty of Social Sciences, Umeå School of Business and Economics (USBE), Statistics.
    Pudas, Sara
    Umeå University, Faculty of Medicine, Department of Integrative Medical Biology (IMB).
    Adolfsson, Rolf
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Psychiatry.
    Kauppi, Karolina
    Umeå University, Faculty of Medicine, Department of Integrative Medical Biology (IMB). Department of Medical Epidemiology and Biostatistics, Karolinska Institute, Solna, Sweden.
    Sex-specific effects of polygenic risk for schizophrenia on lifespan cognitive functioning in healthy individuals2021In: Translational Psychiatry, E-ISSN 2158-3188, Vol. 11, no 1, article id 520Article in journal (Refereed)
    Abstract [en]

    Polygenic risk for schizophrenia has been associated with lower cognitive ability and age-related cognitive change in healthy individuals. Despite well-established neuropsychological sex differences in schizophrenia patients, genetic studies on sex differences in schizophrenia in relation to cognitive phenotypes are scarce. Here, we investigated whether the effect of a polygenic risk score (PRS) for schizophrenia on childhood, midlife, and late-life cognitive function in healthy individuals is modified by sex, and if PRS is linked to accelerated cognitive decline. Using a longitudinal data set from healthy individuals aged 25–100 years (N = 1459) spanning a 25-year period, we found that PRS was associated with lower cognitive ability (episodic memory, semantic memory, visuospatial ability), but not with accelerated cognitive decline. A significant interaction effect between sex and PRS was seen on cognitive task performance, and sex-stratified analyses showed that the effect of PRS was male-specific. In a sub-sample, we observed a male-specific effect of the PRS on school performance at age 12 (N = 496). Our findings of sex-specific effects of schizophrenia genetics on cognitive functioning across the lifespan indicate that the effects of underlying disease genetics on cognitive functioning is dependent on biological processes that differ between the sexes.

    Download full text (pdf)
    fulltext
  • 12. Lindner, P.
    et al.
    Savic, I.
    Sitnikov, R.
    Budhiraja, M.
    Liu, Y.
    Jokinen, Jussi
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Psychiatry. 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 maltreatment2016In: Translational Psychiatry, E-ISSN 2158-3188, Vol. 6, article id e714Article in journal (Refereed)
    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.

    Download full text (pdf)
    fulltext
  • 13. Månsson, Kristoffer N. T.
    et al.
    Lindqvist, Daniel
    Yang, Liu L.
    Svanborg, Cecilia
    Isung, Josef
    Nilsonne, Gustav
    Bergman-Nordgren, Lise
    El Alaoui, Samir
    Hedman-Lagerlöf, Erik
    Kraepelien, Martin
    Högström, Jens
    Andersson, Gerhard
    Boraxbekk, Carl-Johan
    Umeå University, Faculty of Social Sciences, Centre for Demographic and Ageing Research (CEDAR). Center for Magnetic Resonance (DRCMR), Centre for Functional and Diagnostic Imaging and Research, Copenhagen University Hospital, Hvidovre, Denmark.
    Fischer, Håkan
    Lavebratt, Catharina
    Wolkowitz, Owen M.
    Furmark, Tomas
    Improvement in indices of cellular protection after psychological treatment for social anxiety disorder2019In: Translational Psychiatry, E-ISSN 2158-3188, Vol. 9, article id 340Article in journal (Refereed)
    Abstract [en]

    Telomere attrition is a hallmark of cellular aging and shorter telomeres have been reported in mood and anxiety disorders. Telomere shortening is counteracted by the enzyme telomerase and cellular protection is also provided by the antioxidant enzyme glutathione peroxidase (GPx). Here, telomerase, GPx, and telomeres were investigated in 46 social anxiety disorder (SAD) patients in a within-subject design with repeated measures before and after cognitive behavioral therapy. Treatment outcome was assessed by the Liebowitz Social Anxiety Scale (self-report), administered three times before treatment to control for time and regression artifacts, and posttreatment. Venipunctures were performed twice before treatment, separated by 9 weeks, and once posttreatment. Telomerase activity and telomere length were measured in peripheral blood mononuclear cells and GPx activity in plasma. All patients contributed with complete data. Results showed that social anxiety symptom severity was significantly reduced from pretreatment to posttreatment (Cohen’s d = 1.46). There were no significant alterations in telomeres or cellular protection markers before treatment onset. Telomere length and telomerase activity did not change significantly after treatment, but an increase in telomerase over treatment was associated with reduced social anxiety. Also, lower pretreatment telomerase activity predicted subsequent symptom improvement. GPx activity increased significantly during treatment, and increases were significantly associated with symptom improvement. The relationships between symptom improvement and putative protective enzymes remained significant also after controlling for body mass index, sex, duration of SAD, smoking, concurrent psychotropic medication, and the proportion of lymphocytes to monocytes. Thus, indices of cellular protection may be involved in the therapeutic mechanisms of psychological treatment for anxiety.

    Download full text (pdf)
    fulltext
  • 14.
    Månsson, Kristoffer NT
    et al.
    Linköping University.
    Frick, Andreas
    Uppsala University.
    Boraxbekk, Carl-Johan
    Umeå University, Faculty of Medicine, Umeå Centre for Functional Brain Imaging (UFBI). Umeå University, Faculty of Social Sciences, Centre for Population Studies (CPS).
    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 learning2015In: Translational Psychiatry, E-ISSN 2158-3188, Vol. 5, article id e530Article in journal (Refereed)
    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.

  • 15. Månsson, Kristoffer
    et al.
    Salami, Alireza
    Umeå University, Faculty of Medicine, Umeå Centre for Functional Brain Imaging (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 University, Faculty of Social Sciences, Centre for Demographic and Ageing Research (CEDAR). Umeå University, Faculty of Medicine, Umeå Centre for Functional Brain Imaging (UFBI).
    Neuroplasticity in response to cognitive behavior therapy for social anxiety disorder2016In: Translational Psychiatry, E-ISSN 2158-3188, Vol. 6, article id e727Article in journal (Refereed)
    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.

    Download full text (pdf)
    fulltext
  • 16. Porcheret, Kate
    et al.
    van Heugten-van der Kloet, Dalena
    Goodwin, Guy M.
    Foster, Russell G.
    Wulff, Katharina
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Diagnostic Radiology. Umeå University, Faculty of Medicine, Department of Molecular Biology (Faculty of Medicine). 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 trauma2019In: Translational Psychiatry, E-ISSN 2158-3188, Vol. 9, article id 104Article in journal (Refereed)
    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.

    Download full text (pdf)
    fulltext
  • 17.
    Stiernman, Louise
    et al.
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Obstetrics and Gynecology.
    Dubol, Manon
    Department of Women's and Children's Health, Science for Life Laboratory, Uppsala University, Uppsala, Sweden.
    Comasco, Erika
    Department of Women's and Children's Health, Science for Life Laboratory, Uppsala University, Uppsala, Sweden.
    Sundström-Poromaa, Inger
    Department of Women's and Children's Health, Uppsala University, Uppsala, Sweden.
    Boraxbekk, Carl-Johan
    Umeå University, Faculty of Medicine, Umeå Centre for Functional Brain Imaging (UFBI). Umeå University, Faculty of Medicine, Department of Radiation Sciences, Diagnostic Radiology. Institute for Clinical Medicine, Faculty of Medical and Health Sciences, University of Copenhagen, Copenhagen, Denmark; Danish Research Centre for Magnetic Resonance (DRCMR), Centre for Functional and Diagnostic Imaging and Research, Copenhagen University Hospital - Amager and Hvidovre, Copenhagen, Denmark; Institute of Sports Medicine Copenhagen (ISMC) and Department of Neurology, Copenhagen University Hospital Bispebjerg, Copenhagen, Denmark.
    Johansson, Inga-Maj
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Obstetrics and Gynecology.
    Bixo, Marie
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Obstetrics and Gynecology.
    Emotion-induced brain activation across the menstrual cycle in individuals with premenstrual dysphoric disorder and associations to serum levels of progesterone-derived neurosteroids2023In: Translational Psychiatry, E-ISSN 2158-3188, Vol. 13, no 1, article id 124Article in journal (Refereed)
    Abstract [en]

    Premenstrual dysphoric disorder (PMDD) is a debilitating disorder characterized by severe mood symptoms in the luteal phase of the menstrual cycle. PMDD symptoms are hypothesized to be linked to an altered sensitivity to normal luteal phase levels of allopregnanolone (ALLO), a GABAA-modulating progesterone metabolite. Moreover, the endogenous 3β-epimer of ALLO, isoallopregnanolone (ISO), has been shown to alleviate PMDD symptoms through its selective and dose-dependent antagonism of the ALLO effect. There is preliminary evidence showing altered recruitment of brain regions during emotion processing in PMDD, but whether this is associated to serum levels of ALLO, ISO or their relative concentration is unknown. In the present study, subjects with PMDD and asymptomatic controls underwent functional magnetic resonance imaging (fMRI) in the mid-follicular and the late-luteal phase of the menstrual cycle. Brain responses to emotional stimuli were investigated and related to serum levels of ovarian steroids, the neurosteroids ALLO, ISO, and their ratio ISO/ALLO. Participants with PMDD exhibited greater activity in brain regions which are part of emotion-processing networks during the late-luteal phase of the menstrual cycle. Furthermore, activity in key regions of emotion processing networks - the parahippocampal gyrus and amygdala - was differentially associated to the ratio of ISO/ALLO levels in PMDD subjects and controls. Specifically, a positive relationship between ISO/ALLO levels and brain activity was found in PMDD subjects, while the opposite was observed in controls. In conclusion, individuals with PMDD show altered emotion-induced brain responses in the late-luteal phase of the menstrual cycle which may be related to an abnormal response to physiological levels of GABAA-active neurosteroids.

    Download full text (pdf)
    fulltext
  • 18. Szatkiewicz, Jin
    et al.
    Crowley, James J.
    Nordin Adolfsson, Annelie
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Psychiatry.
    Åberg, Karolina A.
    Alaerts, Maaike
    Genovese, Giulio
    McCarroll, Steven
    Del-Favero, Jurgen
    Adolfsson, Rolf
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Psychiatry.
    Sullivan, Patrick F.
    The genomics of major psychiatric disorders in a large pedigree from Northern Sweden2019In: Translational Psychiatry, E-ISSN 2158-3188, Vol. 9, article id 60Article in journal (Refereed)
    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.

    Download full text (pdf)
    fulltext
  • 19.
    Sønderby, Ida E.
    et al.
    NORMENT, Division of Mental Health and Addiction, Oslo University Hospital and Institute of Clinical Medicine, University of Oslo, Oslo, Norway; Department of Medical Genetics, Oslo University Hospital, Oslo, Norway; KG Jebsen Centre for Neurodevelopmental Disorders, University of Oslo, Oslo, Norway.
    van der Meer, Dennis
    NORMENT, Division of Mental Health and Addiction, Oslo University Hospital and Institute of Clinical Medicine, University of Oslo, Oslo, Norway; School of Mental Health and Neuroscience, Faculty of Health, Medicine and Life Sciences, Maastricht University, Maastricht, Netherlands.
    Moreau, Clara
    Sainte Justine Hospital Research Center, QC, Montreal, Canada; Centre de recherche de l'Institut universitaire de gériatrie de Montréal, QC, Montreal, Canada.
    Kaufmann, Tobias
    NORMENT, Division of Mental Health and Addiction, Oslo University Hospital and Institute of Clinical Medicine, University of Oslo, Oslo, Norway; Department of Psychiatry and Psychotherapy, University of Tübingen, Tübingen, Germany.
    Walters, G Bragi
    deCODE Genetics (Amgen), Reykjavík, Iceland; Faculty of Medicine, University of Iceland, Reykjavík, Iceland.
    Ellegaard, Maria
    Department of Clinical Biochemistry, Copenhagen University Hospital, Rigshospitalet, Glostrup, Denmark.
    Abdellaoui, Abdel
    Department of Psychiatry, University of Amsterdam, Amsterdam, Netherlands; Department of Biological Psychology and Netherlands Twin Register, VU University Amsterdam, Amsterdam, Netherlands.
    Ames, David
    University of Melbourne Academic Unit for Psychiatry of Old Age, Kew, Australia; National Ageing Research Institute, Parkville, Australia.
    Amunts, Katrin
    Institute of Neuroscience and Medicine, INM-1, Research Centre Jülich, Jülich, Germany; C. and O. Vogt Institute for Brain Research, Medical Faculty, University Hospital Düsseldorf, Heinrich Heine University Duesseldorf, Düsseldorf, Germany.
    Andersson, Micael
    Umeå University, Faculty of Medicine, Umeå Centre for Functional Brain Imaging (UFBI). Umeå University, Faculty of Medicine, Department of Integrative Medical Biology (IMB).
    Armstrong, Nicola J.
    Murdoch University, Mathematics and Statistics, Perth, Australia.
    Bernard, Manon
    Research Institute, Hospital for Sick Children, ON, Toronto, Canada.
    Blackburn, Nicholas B.
    South Texas Diabetes and Obesity Institute, Department of Human Genetics, School of Medicine, University of Texas Rio Grande Valley, Brownsville, United States.
    Blangero, John
    South Texas Diabetes and Obesity Institute, Department of Human Genetics, School of Medicine, University of Texas Rio Grande Valley, Brownsville, United States.
    Boomsma, Dorret I.
    Department of Biological Psychology and Netherlands Twin Register, VU University Amsterdam, Amsterdam, Netherlands; Amsterdam Neuroscience, Amsterdam, Netherlands; Amsterdam Public Health Research Institute, VU Medical Center, Amsterdam, Netherlands.
    Brodaty, Henry
    Centre for Healthy Brain Ageing, School of Psychiatry, University of New South Wales, Sydney, Australia; Dementia Centre for Research Collaboration, School of Psychiatry, University of New South Wales, Sydney, Australia.
    Brouwer, Rachel M.
    Department of Psychiatry, University Medical Center Brain Center, Utrecht University, Utrecht, Netherlands.
    Bülow, Robin
    Institute of Diagnostic Radiology and Neuroradiology, Greifswald, University Medicine Greifswald, Germany.
    Bøen, Rune
    NORMENT, Division of Mental Health and Addiction, Oslo University Hospital and Institute of Clinical Medicine, University of Oslo, Oslo, Norway; Department of Medical Genetics, Oslo University Hospital, Oslo, Norway.
    Cahn, Wiepke
    Department of Psychiatry, University Medical Center Brain Center, Utrecht University, Utrecht, Netherlands; Altrecht Science, Utrecht, Netherlands.
    Calhoun, Vince D.
    Tri-institutional Center for Translational Research in Neuroimaging and Data Science (TReNDS), Georgia State University, Georgia Institute of Technology, Emory University, Atlanta, United States; Department of Electrical and Computer Engineering, University of New Mexico, Albuquerque, United States.
    Caspers, Svenja
    Institute of Neuroscience and Medicine, INM-1, Research Centre Jülich, Jülich, Germany; Medical Faculty, Heinrich Heine University Düsseldorf, Düsseldorf, Germany.
    Ching, Christopher R K
    Imaging Genetics Center, Mark and Mary Stevens Institute for Neuroimaging and Informatics, University of Southern California, Los Angeles, United States.
    Cichon, Sven
    Institute of Neuroscience and Medicine, INM-1, Research Centre Jülich, Jülich, Germany; Department of Biomedicine, University of Basel, Basel, Switzerland; Institute of Medical Genetics and Pathology, University Hospital Basel, Basel, Switzerland.
    Ciufolini, Simone
    Department of Psychosis Studies, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, United Kingdom.
    Crespo-Facorro, Benedicto
    University Hospital Marqués de Valdecilla, IDIVAL, Centro de Investigación Biomédica en Red Salud Mental (CIBERSAM), Santander, Spain; University Hospital Virgen del Rocío, IBiS, Centre de Investigació Biomédica en Red Salud Mental (CIBERSAM), Sevilla, Spain.
    Curran, Joanne E.
    South Texas Diabetes and Obesity Institute, Department of Human Genetics, School of Medicine, University of Texas Rio Grande Valley, Brownsville, United States.
    Dale, Anders M.
    Center for Multimodal Imaging and Genetics, University of California, San Diego, United States.
    Dalvie, Shareefa
    Department of Psychiatry and Neuroscience Institute, University of Cape Town, Western Cape, Cape Town, South Africa.
    Dazzan, Paola
    Department of Psychological Medicine, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, United Kingdom.
    de Geus, Eco J C
    Department of Biological Psychology and Netherlands Twin Register, VU University Amsterdam, Amsterdam, Netherlands; Amsterdam Neuroscience, Amsterdam, Netherlands; Amsterdam Public Health Research Institute, VU Medical Center, Amsterdam, Netherlands.
    de Zubicaray, Greig I.
    Faculty of Health, Queensland University of Technology, Brisbane, Australia.
    de Zwarte, Sonja M C
    Department of Psychiatry, University Medical Center Brain Center, Utrecht University, Utrecht, Netherlands.
    Desrivieres, Sylvane
    Social, Genetic & Developmental Psychiatry Centre, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, United Kingdom.
    Doherty, Joanne L.
    MRC Centre for Neuropsychiatric Genetics and Genomics, Cardiff University, Cardiff, United Kingdom; Cardiff University Brain Research Imaging Centre School of Psychology, Cardiff University, Cardiff, United Kingdom.
    Donohoe, Gary
    Centre for Neuroimaging and Cognitive Genomics, School of Psychology and Discipline of Biochemistry, National University of Ireland Galway, Galway, Ireland.
    Draganski, Bogdan
    Laboratory for Research in Neuroimaging LREN, Centre for Research in Neurosciences, Department of Clinical Neurosciences, Lausanne University Hospital and University of Lausanne, Lausanne, Switzerland; Neurology Department, Max-Planck-Institute for Human Cognitive and Brain Sciences, Leipzig, Germany.
    Ehrlich, Stefan
    Division of Psychological and Social Medicine, Faculty of Medicine, TU Dresden, Dresden, Germany.
    Eising, Else
    Language and Genetics Department, Max Planck Institute for Psycholinguistics, Nijmegen, Netherlands.
    Espeseth, Thomas
    Department of Psychology, University of Oslo, Oslo, Norway; Bjørknes College, Oslo, Norway.
    Fejgin, Kim
    Signal Transduction, H. Lundbeck A/S ,Ottiliavej 9, Denmark.
    Fisher, Simon E.
    Language and Genetics Department, Max Planck Institute for Psycholinguistics, Nijmegen, Netherlands; Donders Institute for Brain, Cognition and Behaviour, Radboud University, Nijmegen, Netherlands.
    Fladby, Tormod
    Department of Neurology, Akershus University Hospital, Norway; Institute of Clinical Medicine, University of Oslo, Campus Ahus, Oslo, Norway.
    Frei, Oleksandr
    NORMENT, Division of Mental Health and Addiction, Oslo University Hospital and Institute of Clinical Medicine, University of Oslo, Oslo, Norway.
    Frouin, Vincent
    Neurospin, Université Paris-SaclayGif-sur-Yvette, CEA, France.
    Fukunaga, Masaki
    Division of Cerebral Integration, National Institute for Physiological Sciences, Okazaki, Japan; Department of Life Science, Sokendai, Japan.
    Gareau, Thomas
    Neurospin, Université Paris-SaclayGif-sur-Yvette, CEA, France.
    Ge, Tian
    Psychiatric and Neurodevelopmental Genetics Unit, Center for Genomic Medicine, Massachusetts General Hospital, MA, Boston, United States; Department of Psychiatry, Massachusetts General Hospital, Harvard Medical School, MA, Boston, United States; Stanley Center for Psychiatric Research, Broad Institute of MIT and Harvard, MA, Cambridge, United States.
    Glahn, David C.
    Boston Children's Hospital, MA, Boston, United States; Institute of Living, CT, Hartford, United States; Harvard Medical School, MA, Boston, United States.
    Grabe, Hans J.
    Department of Psychiatry and Psychotherapy, Greifswald, University Medicine Greifswald, Germany; German Center of Neurodegenerative Diseases (DZNE), Rostock/Greifswald, Greifswald, Germany.
    Groenewold, Nynke A.
    Department of Psychiatry and Neuroscience Institute, University of Cape Town, Western Cape, Cape Town, South Africa.
    Gústafsson, Ómar
    deCODE Genetics (Amgen), Reykjavík, Iceland.
    Haavik, Jan
    Department of Biomedicine, University of Bergen, Bergen, Norway; Division of Psychiatry, Haukeland University Hospital, Bergen, Norway.
    Haberg, Asta K.
    Department of Neuromedicine and Movement Science, Norwegian University of Science and Technology, Trondheim, Norway; St Olav's Hospital, Department of Radiology and Nuclear Medicine, Trondheim, Norway.
    Hall, Jeremy
    MRC Centre for Neuropsychiatric Genetics and Genomics, Cardiff University, Cardiff, United Kingdom; School of Medicine, Cardiff University, Cardiff, United Kingdom.
    Hashimoto, Ryota
    Department of Pathology of Mental Diseases, National Institute of Mental Health, National Center of Neurology and Psychiatry, Kodaira, Japan; Osaka University, Osaka, Japan.
    Hehir-Kwa, Jayne Y.
    Princess Màxima Center for Pediatric Oncology, Utrecht, Netherlands.
    Hibar, Derrek P.
    Genentech, Inc., South San Francisco, 94080, CA, USA.
    Hillegers, Manon H J
    Department of Child and Adolescent Psychiatry/Psychology, Erasmus MC-Sophia, Rotterdam, Netherlands.
    Hoffmann, Per
    Institute of Medical Genetics and Pathology, University Hospital Basel, Basel, Switzerland; Institute of Human Genetics, University of Bonn Medical School, Bonn, Germany.
    Holleran, Laurena
    Centre for Neuroimaging and Cognitive Genomics, School of Psychology and Discipline of Biochemistry, National University of Ireland Galway, Galway, Ireland.
    Holmes, Avram J.
    Psychology Department, Yale University, CT, New Haven, United States; Department of Psychiatry, Yale University, CT, New Haven, United States; Department of Psychiatry, Massachusetts General Hospital, MA, Boston, United States.
    Homuth, Georg
    Interfaculty Institute for Genetics and Functional Genomics, Greifswald, University Medicine Greifswald, Germany.
    Hottenga, Jouke-Jan
    Department of Biological Psychology and Netherlands Twin Register, VU University Amsterdam, Amsterdam, Netherlands; Amsterdam Neuroscience, Amsterdam, Netherlands; Amsterdam Public Health Research Institute, VU Medical Center, Amsterdam, Netherlands.
    Hulshoff Pol, Hilleke E.
    Department of Psychiatry, University Medical Center Brain Center, Utrecht University, Utrecht, Netherlands.
    Ikeda, Masashi
    Department of Psychiatry, Fujita Health University School of Medicine, Toyoake, Japan.
    Jahanshad, Neda
    Imaging Genetics Center, Mark and Mary Stevens Institute for Neuroimaging and Informatics, University of Southern California, Los Angeles, United States.
    Jockwitz, Christiane
    Institute of Neuroscience and Medicine, INM-1, Research Centre Jülich, Jülich, Germany; Medical Faculty, Heinrich Heine University Düsseldorf, Düsseldorf, Germany.
    Johansson, Stefan
    Department of Clinical Science, University of Bergen, Bergen, Norway; Department of Medical Genetics, Haukeland University Hospital, Bergen, Norway.
    Jönsson, Erik G.
    Centre for Psychiatry Research, Department of Clinical Neuroscience, Karolinska Institutet, Stockholm Health Care Services, Stockholm Region, Stockholm, Sweden; Norwegian Centre for Mental Disorders Research (NORMENT), Institute of Clinical Medicine, University of Oslo, Oslo, Norway.
    Jørgensen, Niklas R.
    Department of Clinical Biochemistry, Copenhagen University Hospital Rigshospitalet, Glostrup, Denmark; Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.
    Kikuchi, Masataka
    Department of Genome Informatics, Graduate School of Medicine, Osaka University, Osaka, Japan.
    Knowles, Emma E M
    Boston Children's Hospital, MA, Boston, United States; Harvard Medical School, MA, Boston, United States.
    Kumar, Kuldeep
    Sainte Justine Hospital Research Center, QC, Montreal, Canada.
    Le Hellard, Stephanie
    Norwegian Centre for Mental Disorders Research, Department of Clinical Science, University of Bergen, Bergen, Norway; Dr Einar Martens Research Group for Biological Psychiatry, Department of Medical Genetics, Haukeland University Hospital, Bergen, Norway.
    Leu, Costin
    Stanley Center for Psychiatric Research, Broad Institute of MIT and Harvard, MA, Cambridge, United States; Genomic Medicine Institute, Lerner Research Institute, Cleveland Clinic, OH, Cleveland, United States; Chalfont Centre for Epilepsy, Chalfont-St-Peter, United Kingdom.
    Linden, David E J
    School of Mental Health and Neuroscience, Faculty of Health, Medicine and Life Sciences, Maastricht University, Maastricht, Netherlands; MRC Centre for Neuropsychiatric Genetics and Genomics, Cardiff University, Cardiff, United Kingdom.
    Liu, Jingyu
    Tri-institutional Center for Translational Research in Neuroimaging and Data Science (TReNDS), Georgia State University, Georgia Institute of Technology, Emory University, Atlanta, United States.
    Lundervold, Arvid
    Department of Biomedicine, University of Bergen, Bergen, Norway; Mohn Medical Imaging and Visualization Centre, Department of Radiology, Haukeland University Hospital, Bergen, Norway.
    Lundervold, Astri Johansen
    Department of Biological and Medical Psychology, University of Bergen, Bergen, Norway.
    Maillard, Anne M.
    Service des Troubles du Spectre de l'Autisme et apparentés, Lausanne University Hospital, Lausanne, Switzerland.
    Martin, Nicholas G.
    Genetic Epidemiology, QIMR Berghofer Medical Research Institute, Brisbane, Australia.
    Martin-Brevet, Sandra
    Laboratory for Research in Neuroimaging LREN, Centre for Research in Neurosciences, Department of Clinical Neurosciences, Lausanne University Hospital and University of Lausanne, Lausanne, Switzerland.
    Mather, Karen A.
    Centre for Healthy Brain Ageing, School of Psychiatry, University of New South Wales, Sydney, Australia; Neuroscience Research Australia, Randwick, Australia.
    Mathias, Samuel R.
    Boston Children's Hospital, MA, Boston, United States; Harvard Medical School, MA, Boston, United States.
    McMahon, Katie L.
    Herston Imaging Research Facility and School of Clinical Sciences, Queensland University of Technology, Brisbane, Australia.
    McRae, Allan F.
    Institute for Molecular Bioscience, University of Queensland, Brisbane, Australia; Queensland Brain Institute, University of Queensland, Brisbane, Australia.
    Medland, Sarah E.
    Psychiatric Genetics, QIMR Berghofer Medical Research Institute, Brisbane, Australia.
    Meyer-Lindenberg, Andreas
    Department of Psychiatry and Psychotherapy, Central Institute of Mental Health, Medical Faculty Mannheim, University of Heidelberg, Mannheim, Germany.
    Moberget, Torgeir
    NORMENT, Division of Mental Health and Addiction, Oslo University Hospital and Institute of Clinical Medicine, University of Oslo, Oslo, Norway; Department of Psychology, University of Oslo, Oslo, Norway.
    Modenato, Claudia
    Laboratory for Research in Neuroimaging LREN, Centre for Research in Neurosciences, Department of Clinical Neurosciences, Lausanne University Hospital and University of Lausanne, Lausanne, Switzerland; University of Lausanne, Lausanne, Switzerland.
    Sánchez, Jennifer Monereo
    Department of Radiology and Nuclear Medicine, Maastricht University Medical Center, Maastricht, Netherlands; School for Mental Health and Neuroscience, Maastricht University, Maastricht, Netherlands.
    Morris, Derek W.
    Centre for Neuroimaging and Cognitive Genomics, School of Psychology and Discipline of Biochemistry, National University of Ireland Galway, Galway, Ireland.
    Mühleisen, Thomas W.
    Institute of Neuroscience and Medicine, INM-1, Research Centre Jülich, Jülich, Germany; C. and O. Vogt Institute for Brain Research, Medical Faculty, University Hospital Düsseldorf, Heinrich Heine University Duesseldorf, Düsseldorf, Germany; Department of Biomedicine, University of Basel, Basel, Switzerland.
    Murray, Robin M.
    Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, United Kingdom.
    Nielsen, Jacob
    Signal Transduction, H. Lundbeck A/S ,Ottiliavej 9, Denmark.
    Nordvik, Jan E.
    CatoSenteret Rehabilitation Center, Son, Norway.
    Nyberg, Lars
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Diagnostic Radiology. Umeå University, Faculty of Medicine, Umeå Centre for Functional Brain Imaging (UFBI). Umeå University, Faculty of Medicine, Department of Integrative Medical Biology (IMB).
    Loohuis, Loes M Olde
    Center for Neurobehavioral Genetics, University of California, Los Angeles, United States.
    Ophoff, Roel A.
    Center for Neurobehavioral Genetics, University of California, Los Angeles, United States; Department of Psychiatry, Erasmus University Medical Center, Rotterdam, Netherlands.
    Owen, Michael J.
    MRC Centre for Neuropsychiatric Genetics and Genomics, Cardiff University, Cardiff, United Kingdom.
    Paus, Tomas
    Bloorview Research Institute, Holland Bloorview Kids Rehabilitation Hospital, ON, Toronto, Canada; Physiology and Nutritional Sciences, University of Toronto, ON, Toronto, Canada.
    Pausova, Zdenka
    Research Institute, Hospital for Sick Children, ON, Toronto, Canada; Physiology and Nutritional Sciences, University of Toronto, ON, Toronto, Canada.
    Peralta, Juan M.
    South Texas Diabetes and Obesity Institute, Department of Human Genetics, School of Medicine, University of Texas Rio Grande Valley, Brownsville, United States.
    Pike, G Bruce
    Departments of Radiology and Clinical Neurosciences, University of Calgary, AB, Calgary, Canada.
    Prieto, Carlos
    Bioinformatics Service, Nucleus, University of Salamanca, Salamanca, Spain.
    Quinlan, Erin B.
    Centre for Population Neuroscience and Precision Medicine, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, United Kingdom.
    Reinbold, Céline S
    Department of Biomedicine, University of Basel, Basel, Switzerland; Institute of Medical Genetics and Pathology, University Hospital Basel, Basel, Switzerland; Department of Psychology, University of Oslo, Oslo, Norway.
    Marques, Tiago Reis
    Department of Psychosis, Institute of Psychiatry, Psychology & Neuroscience, Kings College, London, United Kingdom; Psychiatric Imaging Group, MRC London Institute of Medical Sciences (LMS), Hammersmith Hospital, Imperial College, London, United Kingdom.
    Rucker, James J H
    Institute of Psychiatry, Psychology and Neuroscience, London, United Kingdom.
    Sachdev, Perminder S.
    Centre for Healthy Brain Ageing, School of Psychiatry, University of New South Wales, Sydney, Australia; Neuropsychiatric Institute, Prince of Wales Hospital, Sydney, Australia.
    Sando, Sigrid B.
    Department of Neuromedicine and Movement Science, Norwegian University of Science and Technology, Trondheim, Norway; University Hospital of Trondheim, Department of Neurology and Clinical Neurophysiology, Trondheim, Norway.
    Schofield, Peter R.
    Neuroscience Research Australia, Sydney, Australia; School of Medical Sciences, University of New South Wales, Sydney, Australia.
    Schork, Andrew J.
    Institute of Biological Psychiatry, Roskilde, Denmark; Translational Genetics Institute (TGEN), AZ, Phoenix, United States.
    Schumann, Gunter
    Centre for Population Neuroscience and Precision Medicine, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, United Kingdom.
    Shin, Jean
    Research Institute, Hospital for Sick Children, ON, Toronto, Canada; Physiology and Nutritional Sciences, University of Toronto, ON, Toronto, Canada.
    Shumskaya, Elena
    Donders Institute for Brain, Cognition and Behaviour, Radboud University, Nijmegen, Netherlands; Department of Human Genetics, Radboud University Medical Center, Nijmegen, Netherlands.
    Silva, Ana I.
    School of Mental Health and Neuroscience, Faculty of Health, Medicine and Life Sciences, Maastricht University, Maastricht, Netherlands; MRC Centre for Neuropsychiatric Genetics and Genomics, Cardiff University, Cardiff, United Kingdom; Cardiff University Brain Research Imaging Centre School of Psychology, Cardiff University, Cardiff, United Kingdom.
    Sisodiya, Sanjay M.
    Chalfont Centre for Epilepsy, Chalfont-St-Peter, United Kingdom.
    Steen, Vidar M.
    Norwegian Centre for Mental Disorders Research, Department of Clinical Science, University of Bergen, Bergen, Norway; Dr Einar Martens Research Group for Biological Psychiatry, Department of Medical Genetics, Haukeland University Hospital, Bergen, Norway.
    Stein, Dan J.
    Department of Psychiatry and Neuroscience Institute, University of Cape Town, South African Medical Research Council Unit on Risk and Resilience in Mental Disorders, Cape Town, South Africa.
    Strike, Lachlan T.
    Queensland Brain Institute, University of Queensland, Brisbane, Australia.
    Suzuki, Ikuo K.
    VIB Center for Brain & Disease Research, Stem Cell and Developmental Neurobiology Lab, Leuven, Belgium; University of Brussels (ULB), Institute of Interdisciplinary Research (IRIBHM) ULB Neuroscience Institute, Brussels, Belgium; University of Tokyo, Department of Biological Sciences, Graduate School of Science, Tokyo, Japan.
    Tamnes, Christian K.
    NORMENT, Division of Mental Health and Addiction, Oslo University Hospital and Institute of Clinical Medicine, University of Oslo, Oslo, Norway; PROMENTA Research Center, Department of Psychology, University of Oslo, Oslo, Norway; Department of Psychiatry, Diakonhjemmet Hospital, Oslo, Norway.
    Teumer, Alexander
    Institute for Community Medicine, Greifswald, University Medicine Greifswald, Germany.
    Thalamuthu, Anbupalam
    Centre for Healthy Brain Ageing, School of Psychiatry, University of New South Wales, Sydney, Australia.
    Tordesillas-Gutiérrez, Diana
    University Hospital Marqués de Valdecilla, IDIVAL, Centro de Investigación Biomédica en Red Salud Mental (CIBERSAM), Santander, Spain; Department of Radiology, Marqués de Valdecilla University Hospital, Valdecilla Biomedical Research Institute IDIVAL, Santander, Spain.
    Uhlmann, Anne
    Department of Psychiatry and Neuroscience Institute, University of Cape Town, Western Cape, Cape Town, South Africa.
    Ulfarsson, Magnus O.
    deCODE Genetics (Amgen), Reykjavík, Iceland; Faculty of Electrical and Computer Engineering, University of Iceland, Reykjavík, Iceland.
    van 't Ent, Dennis
    Department of Biological Psychology and Netherlands Twin Register, VU University Amsterdam, Amsterdam, Netherlands; Amsterdam Neuroscience, Amsterdam, Netherlands.
    van den Bree, Marianne B M
    MRC Centre for Neuropsychiatric Genetics and Genomics, Cardiff University, Cardiff, United Kingdom; School of Medicine, Cardiff University, Cardiff, United Kingdom.
    Vanderhaeghen, Pierre
    VIB-KU Leuven Center for Brain & Disease Research, Leuven, Belgium; KU Leuven, Department of Neurosciences & Leuven Brain Institute, Leuven, Belgium; Université Libre de Bruxelles (U.L.B.), Institut de Recherches en Biologie Humaine et Moléculaire (IRIBHM), ULB Neuroscience Institute (UNI), Brussels, Belgium.
    Vassos, Evangelos
    Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, United Kingdom; National Institute for Health Research, Mental Health Biomedical Research Centre, South London and Maudsley National Health Service Foundation Trust and King's College London, London, United Kingdom.
    Wen, Wei
    Centre for Healthy Brain Ageing, School of Psychiatry, University of New South Wales, Sydney, Australia.
    Wittfeld, Katharina
    Department of Psychiatry and Psychotherapy, Greifswald, University Medicine Greifswald, Germany; German Center of Neurodegenerative Diseases (DZNE), Rostock/Greifswald, Greifswald, Germany.
    Wright, Margaret J.
    Queensland Brain Institute, University of Queensland, Brisbane, Australia; Centre for Advanced Imaging, University of Queensland, Brisbane, Australia.
    Agartz, Ingrid
    Centre for Psychiatry Research, Department of Clinical Neuroscience, Karolinska Institutet, Stockholm Health Care Services, Stockholm Region, Stockholm, Sweden; Norwegian Centre for Mental Disorders Research (NORMENT), Institute of Clinical Medicine, University of Oslo, Oslo, Norway; Department of Psychiatry, Diakonhjemmet Hospital, Oslo, Norway.
    Djurovic, Srdjan
    Department of Medical Genetics, Oslo University Hospital, Oslo, Norway; Norwegian Centre for Mental Disorders Research, Department of Clinical Science, University of Bergen, Bergen, Norway.
    Westlye, Lars T.
    NORMENT, Division of Mental Health and Addiction, Oslo University Hospital and Institute of Clinical Medicine, University of Oslo, Oslo, Norway; Department of Psychology, University of Oslo, Oslo, Norway; KG Jebsen Centre for Neurodevelopmental Disorders, University of Oslo, Oslo, Norway.
    Stefansson, Hreinn
    deCODE Genetics (Amgen), Reykjavík, Iceland.
    Stefansson, Kari
    deCODE Genetics (Amgen), Reykjavík, Iceland; Faculty of Medicine, University of Iceland, Reykjavík, Iceland.
    Jacquemont, Sébastien
    Sainte Justine Hospital Research Center, QC, Montreal, Canada; Department of Pediatrics, University of Montreal, QC, Montreal, Canada.
    Thompson, Paul M.
    Imaging Genetics Center, Mark and Mary Stevens Institute for Neuroimaging and Informatics, University of Southern California, Los Angeles, United States.
    Andreassen, Ole A.
    NORMENT, Division of Mental Health and Addiction, Oslo University Hospital and Institute of Clinical Medicine, University of Oslo, Oslo, Norway.
    1q21.1 distal copy number variants are associated with cerebral and cognitive alterations in humans2021In: Translational Psychiatry, E-ISSN 2158-3188, Vol. 11, no 1, article id 182Article in journal (Refereed)
    Abstract [en]

    Low-frequency 1q21.1 distal deletion and duplication copy number variant (CNV) carriers are predisposed to multiple neurodevelopmental disorders, including schizophrenia, autism and intellectual disability. Human carriers display a high prevalence of micro- and macrocephaly in deletion and duplication carriers, respectively. The underlying brain structural diversity remains largely unknown. We systematically called CNVs in 38 cohorts from the large-scale ENIGMA-CNV collaboration and the UK Biobank and identified 28 1q21.1 distal deletion and 22 duplication carriers and 37,088 non-carriers (48% male) derived from 15 distinct magnetic resonance imaging scanner sites. With standardized methods, we compared subcortical and cortical brain measures (all) and cognitive performance (UK Biobank only) between carrier groups also testing for mediation of brain structure on cognition. We identified positive dosage effects of copy number on intracranial volume (ICV) and total cortical surface area, with the largest effects in frontal and cingulate cortices, and negative dosage effects on caudate and hippocampal volumes. The carriers displayed distinct cognitive deficit profiles in cognitive tasks from the UK Biobank with intermediate decreases in duplication carriers and somewhat larger in deletion carriers-the latter potentially mediated by ICV or cortical surface area. These results shed light on pathobiological mechanisms of neurodevelopmental disorders, by demonstrating gene dose effect on specific brain structures and effect on cognitive function.

    Download full text (pdf)
    fulltext
  • 20.
    Tripathi, Anushree
    et al.
    Institute of Psychiatry and Neurosciences of Paris (IPNP), INSERM U1266, Pathophysiology of Psychiatric Disorders, Université de Paris.
    Spedding, Michael
    Schenker, Esther
    Didriksen, Michael
    Cressant, Arnaud
    Jay, Therese M.
    Cognition- and circuit-based dysfunction in a mouse model of 22q11.2 microdeletion syndrome: effects of stress2020In: Translational Psychiatry, E-ISSN 2158-3188, Vol. 10, no 1, article id 41Article in journal (Refereed)
    Abstract [en]

    Genetic microdeletion at the 22q11 locus is associated with very high risk for schizophrenia. The 22q11.2 microdeletion (Df(h22q11)/+) mouse model shows cognitive deficits observed in this disorder, some of which can be linked to dysfunction of the prefrontal cortex (PFC). We used behavioral (n = 10 per genotype), electrophysiological (n = 7 per genotype per group), and neuroanatomical (n = 5 per genotype) techniques to investigate schizophrenia-related pathology of Df(h22q11)/+ mice, which showed a significant decrease in the total number of parvalbumin positive interneurons in the medial PFC. The Df(h22q11)/+ mice when tested on PFC-dependent behavioral tasks, including gambling tasks, perform significantly worse than control animals while exhibiting normal behavior on hippocampus-dependent tasks. They also show a significant decrease in hippocampus-medial Prefrontal cortex (H-PFC) synaptic plasticity (long-term potentiation, LTP). Acute platform stress almost abolished H-PFC LTP in both wild-type and Df(h22q11)/+ mice. H-PFC LTP was restored to prestress levels by clozapine (3 mg/kg i.p.) in stressed Df(h22q11)/+ mice, but the restoration of stress-induced LTP, while significant, was similar between wild-type and Df(h22q11)/+ mice. A medial PFC dysfunction may underlie the negative and cognitive symptoms in human 22q11 deletion carriers, and these results are relevant to the current debate on the utility of clozapine in such subjects.

    Download full text (pdf)
    fulltext
  • 21. 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 University, Faculty of Medicine, Department of Clinical Sciences, Psychiatry.
    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 schizophrenia2017In: Translational Psychiatry, E-ISSN 2158-3188, Vol. 7, article id e1155Article in journal (Refereed)
    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.

    Download full text (pdf)
    fulltext
1 - 21 of 21
CiteExportLink to result list
Permanent link
Cite
Citation style
  • apa
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf