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  • 1.
    Ollila, Hanna M.
    et al.
    Institute for Molecular Medicine Finland (FIMM), University of Helsinki, Finland ; Center for Genomic Medicine, Massachusetts General Hospital, Boston, MA, United States ; Program in Medical and Population Genetics, Broad Institute, Cambridge, MA, United States ; Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA, United States.
    Sinnott-Armstrong, Nasa
    Department of Genetics, School of Medicine, Stanford University, CA, United States.
    Kantojärvi, Katri
    Population Health, Finnish Institute for Health and Welfare, Helsinki, Finland ; Department of Psychiatry and SleepWell Research Program, Faculty of Medicine, University of Helsinki and Helsinki University Central Hospital, Finland.
    Broberg, Martin
    Institute for Molecular Medicine Finland (FIMM), University of Helsinki, Finland.
    Palviainen, Teemu
    Institute for Molecular Medicine Finland (FIMM), University of Helsinki, Finland.
    Jones, Samuel
    Institute for Molecular Medicine Finland (FIMM), University of Helsinki, Finland.
    Ripatti, Vili
    Institute for Molecular Medicine Finland (FIMM), University of Helsinki, Finland.
    Pandit, Anita
    Department of Biostatistics, School of Public Health, University of Michigan, Ann Arbor, MI, United States.
    Rong, Robin
    Department of Biostatistics, School of Public Health, University of Michigan, Ann Arbor, MI, United States.
    Kristiansson, Kati
    Population Health, Finnish Institute for Health and Welfare, Helsinki, Finland.
    Sandman, Nils
    Department of Psychology and Speech-Language Pathology, and Turku Brain and Mind Center, University of Turku, Finland.
    Valli, Katja
    University of Skövde, School of Bioscience. University of Skövde, Systems Biology Research Environment. Department of Psychology and Speech-Language Pathology, and Turku Brain and Mind Center, University of Turku, Finland.
    Hublin, Christer
    Finnish Institute of Occupational Health, Helsinki, Finland.
    Ripatti, Samuli
    Institute for Molecular Medicine Finland (FIMM), University of Helsinki, Finland ; Center for Genomic Medicine, Massachusetts General Hospital, Boston, MA, United States ; Program in Medical and Population Genetics, Broad Institute, Cambridge, MA, United States.
    Widen, Elisabeth
    Institute for Molecular Medicine Finland (FIMM), University of Helsinki, Finland.
    Kaprio, Jaakko
    Institute for Molecular Medicine Finland (FIMM), University of Helsinki, Finland.
    Saxena, Richa
    Center for Genomic Medicine, Massachusetts General Hospital, Boston, MA, United States ; Program in Medical and Population Genetics, Broad Institute, Cambridge, MA, United States ; Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA, United States ; Division of Sleep and Circadian Disorders, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA, United States.
    Paunio, Tiina
    Population Health, Finnish Institute for Health and Welfare, Helsinki, Finland ; Department of Psychiatry and SleepWell Research Program, Faculty of Medicine, University of Helsinki and Helsinki University Central Hospital, Finland.
    Nightmares share genetic risk factors with sleep and psychiatric traits2024In: Translational Psychiatry, E-ISSN 2158-3188, Vol. 14, no 1, article id 123Article in journal (Refereed)
    Abstract [en]

    Nightmares are vivid, extended, and emotionally negative or negative dreams that awaken the dreamer. While sporadic nightmares and bad dreams are common and generally harmless, frequent nightmares often reflect underlying pathologies of emotional regulation. Indeed, insomnia, depression, anxiety, or alcohol use have been associated with nightmares in epidemiological and clinical studies. However, the connection between nightmares and their comorbidities are poorly understood. Our goal was to examine the genetic risk factors for nightmares and estimate correlation or causality between nightmares and comorbidities. We performed a genome-wide association study (GWAS) in 45,255 individuals using a questionnaire-based assessment on the frequency of nightmares during the past month and genome-wide genotyping data. While the GWAS did not reveal individual risk variants, heritability was estimated at 5%. In addition, the genetic correlation analysis showed a robust correlation (rg > 0.4) of nightmares with anxiety (rg = 0.671, p = 7.507e−06), depressive (rg = 0.562, p = 1.282e−07) and posttraumatic stress disorders (rg = 0.4083, p = 0.0152), and personality trait neuroticism (rg = 0.667, p = 4.516e−07). Furthermore, Mendelian randomization suggested causality from insomnia to nightmares (beta = 0.027, p = 0.0002). Our findings suggest that nightmares share genetic background with psychiatric traits and that insomnia may increase an individual’s liability to experience frequent nightmares. Given the significant correlations with psychiatric and psychological traits, it is essential to grow awareness of how nightmares affect health and disease and systematically collect information about nightmares, especially from clinical samples and larger cohorts. 

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  • 2.
    Risal, Sanjiv
    et al.
    Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
    Manti, Maria
    Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
    Lu, Haojiang
    Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
    Fornes, Romina
    Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
    Larsson, Henrik
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden / School of Medical Sciences, Örebro University, Sweden.
    Benrick, Anna
    University of Skövde, School of Health Sciences. University of Skövde, Digital Health Research (DHEAR). Department of Physiology, Sahlgrenska Academy, University of Gothenburg, Sweden.
    Deng, Quiaolin
    Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
    Cesta, Carolyn E.
    Department of Medicine, Solna, Centre for Pharmacoepidemiology, Karolinska Institutet, Stockholm, Sweden.
    Rosenqvist, Mina A.
    School of Medical Sciences, Örebro University, Sweden.
    Stener-Victorin, Elisabet
    Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
    Prenatal androgen exposure causes a sexually dimorphic transgenerational increase in offspring susceptibility to anxiety disorders2021In: Translational Psychiatry, E-ISSN 2158-3188, Vol. 11, no 1, article id 45Article in journal (Refereed)
    Abstract [en]

    If and how obesity and elevated androgens in women with polycystic ovary syndrome (PCOS) affect their offspring’s psychiatric health is unclear. Using data from Swedish population health registers, we showed that daughters of mothers with PCOS have a 78% increased risk of being diagnosed with anxiety disorders. We next generated a PCOS-like mouse (F0) model induced by androgen exposure during late gestation, with or without diet-induced maternal obesity, and showed that the first generation (F1) female offspring develop anxiety-like behavior, which is transgenerationally transmitted through the female germline into the third generation of female offspring (F3) in the androgenized lineage. In contrast, following the male germline, F3 male offspring (mF3) displayed anxiety-like behavior in the androgenized and the obese lineages. Using a targeted approach to search for molecular targets within the amygdala, we identified five differentially expressed genes involved in anxiety-like behavior in F3 females in the androgenized lineage and eight genes in the obese lineage. In mF3 male offspring, three genes were dysregulated in the obese lineage but none in the androgenized lineage. Finally, we performed in vitro fertilization (IVF) using a PCOS mouse model of continuous androgen exposure. We showed that the IVF generated F1 and F2 offspring in the female germline did not develop anxiety-like behavior, while the F2 male offspring (mF2) in the male germline did. Our findings provide evidence that elevated maternal androgens in PCOS and maternal obesity may underlie the risk of a transgenerational transmission of anxiety disorders in children of women with PCOS.

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