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  • 1.
    Aardal-Eriksson, Elisabeth
    et al.
    Linköpings universitet, Institutionen för biomedicin och kirurgi, Klinisk kemi. Linköpings universitet, Hälsouniversitetet.
    Eriksson, Thomas E.
    Linköpings universitet, Institutionen för nervsystem och rörelseorgan, Psykiatri. Linköpings universitet, Hälsouniversitetet.
    Thorell, Lars-Håkan
    Linköpings universitet, Institutionen för nervsystem och rörelseorgan, Psykiatri. Linköpings universitet, Hälsouniversitetet.
    Salivary cortisol, posttraumatic stress symptoms, and general health in the acute phase and during 9-month follow-up2001Inngår i: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 50, nr 12, s. 986-993Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: Because traumatic events are unpredictable, there are few studies of psychobiological states immediately following such events. Our study aimed to determine the relation of salivary cortisol to psychologic distress immediately after a traumatic event and then during follow-up.

    Methods: Measurement of morning and evening salivary cortisol and ratings of psychologic distress (using the Impact of Events Scale [IES], the Post Traumatic Symptom Scale, and the General Health Questionnaire) were performed with 31 United Nations soldiers at three time points—5 days and 2 and 9 months—following a mine accident in Lebanon.

    Results: Five days after the accident, 15 subjects reported substantial posttraumatic distress according to the IES, as well as significantly lower morning and higher evening cortisol levels compared with the low-impact group. Within 9 months, the posttraumatic distress of the high-impact group was reduced, accompanied by an increase in morning and a decrease in evening cortisol levels. There were significant relationships between evening cortisol and all rating scales at the first and third time points.

    Conclusions: Subclinical posttraumatic stress following an adverse event can be measured biologically via salivary cortisol levels soon after the event.

  • 2.
    Aardal-Eriksson, Elisabeth
    et al.
    Linköpings universitet, Institutionen för biomedicin och kirurgi, Klinisk kemi. Linköpings universitet, Hälsouniversitetet.
    Eriksson, Thomas
    Linköpings universitet, Institutionen för nervsystem och rörelseorgan, Psykiatri. Linköpings universitet, Hälsouniversitetet.
    Holm, Ann-Charlotte
    Linköpings universitet, Institutionen för biomedicin och kirurgi, Klinisk kemi. Linköpings universitet, Hälsouniversitetet.
    Lundin, Tom
    Department of Psychiatry, Uppsala Academic Hospital, Uppsala University, Uppsala (TL), Sweden.
    Salivary cortisol and serum prolactin in relation to stress rating scales in a group of rescue workers1999Inngår i: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 46, nr 6, s. 850-855Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: Rescue service personnel are often exposed to traumatic events as part of their occupation, and higher prevalence rates of psychiatric illness have been found among this group.

    Methods: In 65 rescue workers, salivary cortisol at 8 am and 10 pm and serum prolactin at 8 am were related to the psychiatric self-rating scale General Health Questionnaire (GHQ-28) measuring psychiatric health, and the Impact of Events Scale (IES) and Post Traumatic Symptom Scale (PTSS) measuring posttraumatic symptoms.

    Results: Seventeen percent of the study population scored above the GHQ-28 cut-off limit but none scored beyond the cut-off limit in the IES and PTSS questionnaires. Salivary cortisol concentration at 10 pm correlated with statistical significance to anxiety (p < .005) and depressive symptoms (p < .01) measured with GHQ-28, as well as to posttraumatic symptoms, with avoidance behavior measured with IES (p < .01) and PTSS (p < .005). Two of the rescue workers were followed over time with the same sampling procedure after a major rescue commission.

    Conclusions: The correlation between evening salivary cortisol and anxiety, depressiveness, and posttraumatic avoidance symptoms indicates that these parameters can be used in screening and follow-up after traumatic stress events.

  • 3.
    Alaie, Iman
    et al.
    Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Frick, Andreas
    Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Engman, Jonas
    Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Björkstrand, Johannes
    Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Faria, Vanda
    Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Gingnell, Malin
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kvinnors och barns hälsa, Obstetrik & gynekologi. Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Wallenquist, Ulrika
    Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Wahlstedt, Kurt
    Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Fredrikson, Mats
    Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Furmark, Tomas
    Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Symptom Improvement in Social Anxiety Disorder is Associated with Reduced Amygdala Reactivity to Emotional Faces2013Inngår i: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 73, nr 9, s. 79S-79SArtikkel i tidsskrift (Annet vitenskapelig)
  • 4.
    Alaie, Iman
    et al.
    Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Frick, Andreas
    Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Marteinsdottir, Ina
    Hartvig, Per
    Tillfors, Maria
    Eriksson, Elias
    Fredrikson, Mats
    Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Furmark, Tomas
    Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Serotonin Synthesis Rate and the Tryptophan Hydroxylase-2 G-703T Polymorphism in Social Anxiety Disorder2014Inngår i: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 75, nr 9, s. 357S-357SArtikkel i tidsskrift (Annet vitenskapelig)
  • 5.
    Alaie, Iman
    et al.
    Dept Psychol, Uppsala Univ, Uppsala, Sweden.
    Frick, Andreas
    Dept Psychol, Uppsala Univ, Uppsala, Sweden.
    Marteinsdottir, Ina
    Dept Clin & Expt Med, Linköping Univ, Linköping, Sweden.
    Hartvig, Per
    Dept Drug Design & Pharmacol, Univ Copenhagen, Copenhagen, Denmark.
    Tillfors, Maria
    Örebro universitet, Institutionen för juridik, psykologi och socialt arbete.
    Eriksson, Elias
    Dept Pharmacol, Univ Gothenburg, Gothenburg, Sweden.
    Fredrikson, Mats
    Dept Psychol, Uppsala Univ, Uppsala, Sweden.
    Furmark, Tomas
    Dept Psychol, Uppsala Univ, Uppsala, Sweden.
    Serotonin Synthesis Rate and the Tryptophan Hydroxylase-2 G-703T Polymorphism in Social Anxiety Disorder2014Inngår i: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 75, nr 9, s. 357S-357SArtikkel i tidsskrift (Annet vitenskapelig)
  • 6.
    Alaie, Iman
    et al.
    Uppsala universitet.
    Frick, Andreas
    Uppsala universitet.
    Marteinsdottir, Ina
    Linköping University.
    Hartvig, Per
    Copenhagen University.
    Tillfors, Maria
    Örebro universitet.
    Eriksson, Elias
    Gothenburg University.
    Fredrikson, Mats
    Uppsala universitet.
    Furmark, Tomas
    Uppsala universitet.
    Serotonin Synthesis Rate and the Tryptophan Hydroxylase-2 G-703T Polymorphism in Social Anxiety Disorder2014Inngår i: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 75, nr 9, s. 357S-357SArtikkel i tidsskrift (Fagfellevurdert)
  • 7.
    Barbier, Estelle
    et al.
    Linköpings universitet, Institutionen för biomedicinska och kliniska vetenskaper, Centrum för social och affektiv neurovetenskap. Linköpings universitet, Medicinska fakulteten.
    Barchiesi, Riccardo
    Linköpings universitet, Institutionen för biomedicinska och kliniska vetenskaper, Centrum för social och affektiv neurovetenskap. Linköpings universitet, Medicinska fakulteten.
    Domi, Ana
    Univ Gothenburg, Sweden.
    Chanthongdee, Kanat
    Linköpings universitet, Institutionen för biomedicinska och kliniska vetenskaper, Centrum för social och affektiv neurovetenskap. Linköpings universitet, Medicinska fakulteten. Mahidol Univ, Thailand.
    Domi, Esi
    Linköpings universitet, Institutionen för biomedicinska och kliniska vetenskaper, Centrum för social och affektiv neurovetenskap. Linköpings universitet, Medicinska fakulteten.
    Augier, Gaëlle
    Linköpings universitet, Institutionen för biomedicinska och kliniska vetenskaper, Centrum för social och affektiv neurovetenskap. Linköpings universitet, Medicinska fakulteten.
    Augier, Eric
    Linköpings universitet, Institutionen för biomedicinska och kliniska vetenskaper, Centrum för social och affektiv neurovetenskap. Linköpings universitet, Medicinska fakulteten.
    Xu, Li
    Linköpings universitet, Institutionen för biomedicinska och kliniska vetenskaper, Centrum för social och affektiv neurovetenskap. Linköpings universitet, Medicinska fakulteten. Sichuan Prov Peoples Hosp, Peoples R China.
    Adermark, Louise
    Univ Gothenburg, Sweden.
    Heilig, Markus
    Linköpings universitet, Institutionen för biomedicinska och kliniska vetenskaper, Centrum för social och affektiv neurovetenskap. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Psykiatricentrum, Psykiatriska kliniken i Linköping.
    Downregulation of Synaptotagmin 1 in the Prelimbic Cortex Drives Alcohol-Associated Behaviors in Rats2021Inngår i: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 89, nr 4, s. 398-406Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND: Alcohol addiction is characterized by persistent neuroadaptations in brain structures involved in motivation, emotion, and decision making, including the medial prefrontal cortex, the nucleus accumbens, and the amygdala. We previously reported that induction of alcohol dependence was associated with long-term changes in the expression of genes involved in neurotransmitter release. Specifically, Syt1, which plays a key role in neurotransmitter release and neuronal functions, was downregulated. Here, we therefore examined the role of Syt1 in alcohol-associated behaviors in rats. METHODS: We evaluated the effect of Syt1 downregulation using an adeno-associated virus (AAV) containing a short hairpin RNA against Syt1. Cre-dependent Syt1 was also used in combination with an rAAV2 retro-Cre virus to assess circuit-specific effects of Syt1 knockdown (KD). RESULTS: Alcohol-induced downregulation of Syt1 is specific to the prelimbic cortex (PL), and KD of Syt1 in the PL resulted in escalated alcohol consumption, increased motivation to consume alcohol, and increased alcohol drinking despite negative consequences ("compulsivity"). Syt1 KD in the PL altered the excitation/inhibition balance in the basolateral amygdala, while the nucleus accumbens core was unaffected. Accordingly, a projection-specific Syt1 KD in the PL-basolateral amygdala projection was sufficient to increase compulsive alcohol drinking, while a KD of Syt1 restricted to PL-nucleus accumbens core projecting neurons had no effect on tested alcohol-related behaviors. CONCLUSIONS: Together, these data suggest that dysregulation of Syt1 is an important mechanism in long-term neuroadaptations observed after a history of alcohol dependence, and that Syt1 regulates alcohol-related behaviors in part by affecting a PL-basolateral amygdala brain circuit.

    Fulltekst (pdf)
    fulltext
  • 8. Bas-Hoogendam, Janna Marie
    et al.
    van Steenbergen, Henk
    Pannekoek, J. Nienke
    Fouche, Jean-Paul
    Lochner, Christine
    Hattingh, Coenraad J.
    Cremers, Henk R.
    Furmark, Tomas
    Månsson, Kristoffer N. T.
    Frick, Andreas
    Engman, Jonas
    Boraxbekk, Carl-Johan
    Umeå universitet, Samhällsvetenskapliga fakulteten, Enheten för demografi och åldrandeforskning (CEDAR).
    Carlbring, Per
    Andersson, Gerhard
    Fredrikson, Mats
    Straube, Thomas
    Peterburs, Jutta
    Klumpp, Heide
    Phan, K. Luan
    Roelofs, Karin
    Stein, Dan J.
    van der Wee, Nic. J. A.
    Sample Size Matters: A Voxel-Based Morphometry Multi-Center Mega-Analysis of Gray Matter Volume in Social Anxiety Disorder2017Inngår i: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 81, nr 10, s. S7-S7Artikkel i tidsskrift (Fagfellevurdert)
  • 9.
    Bas-Hoogendam, Janna Marie
    et al.
    Leiden Univ, Leiden, Netherlands..
    van Steenbergen, Henk
    Leiden Univ, Leiden, Netherlands..
    Pannekoek, J. Nienke
    Imperial Coll London, London, England..
    Fouche, Jean-Paul
    Univ Cape Town, Rondebosch, South Africa..
    Lochner, Christine
    Stellenbosch Univ, Stellenbosch, South Africa..
    Hattingh, Coenraad J.
    Univ Cape Town, Rondebosch, South Africa..
    Cremers, Henk R.
    Univ Amsterdam, Amsterdam, Netherlands..
    Furmark, Tomas
    Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Månsson, Kristoffer N. T.
    Linkoping Univ, Linkoping, Sweden..
    Frick, Andreas
    Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Engman, Jonas
    Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Boraxbekk, Carl-Johan
    Umea Univ, Umea, Sweden..
    Carlbring, Per
    Stockholm Univ, Stockholm, Sweden..
    Andersson, Gerhard
    Linkoping Univ, Linkoping, Sweden..
    Fredriksson, Mats
    Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Straube, Thomas
    Univ Munster, Munster, Germany..
    Peterburs, Jutta
    Univ Munster, Munster, Germany..
    Klumpp, Heide
    Univ Illinois, Chicago, IL USA..
    Phan, K. Luan
    Univ Illinois, Chicago, IL USA..
    Roelofs, Karin
    Radboud Univ Nijmegen, Nijmegen, Netherlands..
    Stein, Dan J.
    Univ Cape Town, Rondebosch, South Africa..
    van der Wee, Nic. J. A.
    Leiden Univ, Med Ctr, Leiden, Netherlands..
    Sample Size Matters: A Voxel-Based Morphometry Multi-Center Mega-Analysis of Gray Matter Volume in Social Anxiety Disorder2017Inngår i: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 81, nr 10, s. S7-S8Artikkel i tidsskrift (Annet vitenskapelig)
  • 10. Bas-Hoogendam, Janna Marie
    et al.
    van Steenbergen, Henk
    Pannekoek, J. Nienke
    Fouche, Jean-Paul
    Lochner, Christine
    Hattingh, Coenraad J.
    Cremers, Henk R.
    Furmark, Tomas
    Månsson, Kristoffer N.T.
    Frick, Andreas
    Engman, Jonas
    Boraxbekk, Carl-Johan
    Carlbring, Per
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Psykologiska institutionen, Klinisk psykologi.
    Sample Size Matters: A Voxel-Based Morphometry Multi-Center Mega-Analysis of Gray Matter Volume in Social Anxiety Disorder2017Inngår i: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 81, nr 10, s. S7-S8Artikkel i tidsskrift (Annet vitenskapelig)
    Abstract [en]

    Background: Social Anxiety Disorder (SAD) is a disabling psychiatric disorder, associated with high co-morbidity. Previous research on structural brain alterations associated with SAD has yielded inconsistent results concerning changes in gray matter (GM) in various brain regions, as well as on the relationship between GM and SAD-symptomatology. These heterogeneous findings are possibly due to limited sample sizes. Multi-site imaging offers new possibilities to investigate SAD-related GM changes in larger samples.

    Methods: An international multi-center mega-analysis on the largest database of SAD brain scans to date was performed to compare GM volumes of SAD-patients (n=174) and healthy participants (n=213) using voxel-based morphometry. A hypothesis-driven region of interest (ROI) approach was used, focusing on the basal ganglia, amygdala-hippocampal complex, prefrontal cortex and parietal cortex.

    Results: SAD-patients had larger GM volume in the dorsal striatum when compared to healthy participants. This increase correlated positively with the level of social anxiety symptoms. No SAD-related differences in GM volume were present in the other ROIs.

    Conclusions: The results suggest a role for the dorsal striatum in SAD, but previously reported SAD-related changes in GM in the amygdala, hippocampus, precuneus, prefrontal cortex and parietal regions were not replicated. Thereby, our findings indicate that sample size matters and stress the need for meta-analyses like those performed by the Enhancing NeuroImaging Genetics through Meta-Analysis (ENIGMA) Consortium and its working groups. Actually, the collaborative effort for this work has resulted in the start of the ENIGMA-Anxiety workgroup.

  • 11.
    Berna, Chantal
    et al.
    Univ Oxford, Dept Clin Neurol, Ctr Funct Magnet Resonance Imaging Brain, Oxford OX3 9DU, England;Univ Oxford, Warneford Hosp, Dept Psychiat, Oxford OX3 9DU, England.
    Leknes, Siri
    Univ Oxford, Dept Clin Neurol, Ctr Funct Magnet Resonance Imaging Brain, Oxford OX3 9DU, England.
    Holmes, Emily A.
    Univ Oxford, Warneford Hosp, Dept Psychiat, Oxford OX3 9DU, England.
    Edwards, Robert R.
    Harvard Univ, Brigham & Womens Hosp, Sch Med, Dept Anesthesiol, Chestnut Hill, MA USA.
    Goodwin, Guy M.
    Univ Oxford, Warneford Hosp, Dept Psychiat, Oxford OX3 9DU, England.
    Tracey, Irene
    Univ Oxford, Dept Clin Neurol, Ctr Funct Magnet Resonance Imaging Brain, Oxford OX3 9DU, England.
    Induction of Depressed Mood Disrupts Emotion Regulation Neurocircuitry and Enhances Pain Unpleasantness2010Inngår i: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 67, nr 11, s. 1083-1090Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: Depressed mood alters the pain experience. Yet, despite its clear clinical relevance, little is known about the cognitive and neural mechanisms underlying this phenomenon. We tested an experimental manipulation to unravel the interaction between depressed mood and pain. We hypothesized that dysregulation of the neural circuitry underlying emotion regulation is the mechanism whereby pain processing is affected during depressed mood. Methods: Using functional magnetic resonance imaging, we compared the effects of sad and neutral cognitive mood inductions on affective pain ratings, pain-specific cognitions, and central pain processing of a tonic noxious heat stimulus in 20 healthy volunteers. Results: The increase in negative pain-specific cognitions during depressed mood predicted the perceived increase in pain unpleasantness. Following depressed mood induction, brain responses to noxious thermal stimuli were characterized by increased activity in a broad network including prefrontal areas, subgenual anterior cingulate cortex, and hippocampus, as well as significantly less deactivation when compared with pain responses in a neutral mood. The participants who reported the largest increase in pain unpleasantness after the sad mood induction showed greater inferior frontal gyrus and amygdala activation, linking changes in emotion regulation mechanisms with enhancement of pain affect. Conclusions: Our results inform how depressed mood and chronic pain co-occur clinically and may serve to develop and translate effective interventions using pharmacological or psychological treatment.

  • 12.
    Bilbao, Ainhoa
    et al.
    University of Heidelberg, Mannheim, Germany.
    Robinson, J Elliott
    Department of Neurology, University of North Carolina School of Medicine, Chapel Hill, North Carolina, USA.
    Heilig, Markus
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för neuro- och inflammationsvetenskap. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Närsjukvården i centrala Östergötland, Psykiatriska kliniken.
    Malanga, C J
    Department of Neurology, University of North Carolina School of Medicine, Chapel Hill, North Carolina, USA.
    Spanagel, Rainer
    University of Heidelberg, Mannheim, Germany.
    Sommer, Wolfgang H
    University of Heidelberg, Mannheim, Germany.
    Thorsell, Annika
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för neuro- och inflammationsvetenskap. Linköpings universitet, Medicinska fakulteten.
    A Pharmacogenetic Determinant of Mu-Opioid Receptor Antagonist Effects on Alcohol Reward and Consumption: Evidence from Humanized Mice.2015Inngår i: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 77, nr 10, s. 850-858Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND: It has been proposed that therapeutic responses to naltrexone in alcoholism are moderated by variation at the mu-opioid receptor gene locus (OPRM1). This remains controversial because human results vary and no prospectively genotyped studies have been reported. We generated humanized mice carrying the respective human OPRM1 A118G alleles. Here, we used this model system to examine the role of OPRM1 A118G variation for opioid antagonist effects on alcohol responses.

    METHODS: Effects of naltrexone on alcohol reward were examined using intracranial self-stimulation. Effects of naltrexone or nalmefene on alcohol intake were examined in continuous access home cage two-bottle free-choice drinking and operant alcohol self-administration paradigms.

    RESULTS: Alcohol lowered brain stimulation reward thresholds in 118GG mice in a manner characteristic of rewarding drugs, and this effect was blocked by naltrexone. Brain stimulation reward thresholds were unchanged by alcohol or naltrexone in 118AA mice. In the home cage, increased alcohol intake emerged in 118GG mice with increasing alcohol concentrations and was 33% higher at 17% alcohol. At this concentration, naltrexone selectively suppressed alcohol intake in 118GG animals to a level virtually identical to that of 118AA mice. No effect of naltrexone was found in the latter group. Similarly, both naltrexone and nalmefene were more effective in suppressing operant alcohol self-administration in 118GG mice.

    CONCLUSIONS: In a model that allows close experimental control, OPRM1 A118G variation robustly moderates effects of opioid antagonism on alcohol reward and consumption. These findings strongly support a personalized medicine approach to alcoholism treatment that takes into account OPRM1 genotype.

  • 13.
    Björkstrand, Johannes
    et al.
    Uppsala Univ, Uppsala, Sweden.;Lund Univ, Lund, Sweden..
    Karlsson, Barry
    Uppsala Univ, Uppsala, Sweden..
    Rosen, Jorgen
    Uppsala Univ, Uppsala, Sweden..
    Olsson, Emil
    Lund Univ, Lund, Sweden..
    Åhs, Fredrik
    Mittuniversitetet, Fakulteten för humanvetenskap, Institutionen för psykologi och socialt arbete.
    Fredrikson, Mats
    Uppsala Univ, Uppsala, Sweden.;Karolinska Inst, Solna, Sweden..
    Frick, Andreas
    Uppsala Univ, Uppsala, Sweden..
    High Unconditioned Stimulus Intensity Results in Stronger Threat Conditioning Than Low Intensity2020Inngår i: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 87, nr 9, s. S181-S181Artikkel i tidsskrift (Fagfellevurdert)
  • 14.
    Björkstrand, Johannes
    et al.
    Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Ågren, Thomas
    Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Furmark, Tomas
    Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Eriksson, Elias
    Fredrikson, Mats
    Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Disruption of Fear Reconsolidation by Extinction and the G-703T Gene Polymorphism2013Inngår i: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 73, nr 9, s. 67S-67SArtikkel i tidsskrift (Annet vitenskapelig)
  • 15. Blokland, Gabriëlla A. M.
    et al.
    Grove, Jakob
    Chen, Chia-Yen
    Cotsapas, Chris
    Tobet, Stuart
    Handa, Robert
    St Clair, David
    Lencz, Todd
    Mowry, Bryan J.
    Periyasamy, Sathish
    Cairns, Murray J.
    Tooney, Paul A.
    Wu, Jing Qin
    Kelly, Brian
    Kirov, George
    Sullivan, Patrick F.
    Corvin, Aiden
    Riley, Brien P.
    Esko, Tõnu
    Milani, Lili
    Jönsson, Erik G.
    Palotie, Aarno
    Ehrenreich, Hannelore
    Begemann, Martin
    Steixner-Kumar, Agnes
    Sham, Pak C.
    Iwata, Nakao
    Weinberger, Daniel R.
    Gejman, Pablo V.
    Sanders, Alan R.
    Buxbaum, Joseph D.
    Rujescu, Dan
    Giegling, Ina
    Konte, Bettina
    Hartmann, Anette M.
    Bramon, Elvira
    Murray, Robin M.
    Pato, Michele T.
    Lee, Jimmy
    Melle, Ingrid
    Molden, Espen
    Ophoff, Roel A.
    McQuillin, Andrew
    Bass, Nicholas J.
    Adolfsson, Rolf
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Malhotra, Anil K.
    Martin, Nicholas G.
    Fullerton, Janice M.
    Mitchell, Philip B.
    Schofield, Peter R.
    Forstner, Andreas J.
    Degenhardt, Franziska
    Schaupp, Sabrina
    Comes, Ashley L.
    Kogevinas, Manolis
    Guzman-Parra, José
    Reif, Andreas
    Streit, Fabian
    Sirignano, Lea
    Cichon, Sven
    Grigoroiu-Serbanescu, Maria
    Hauser, Joanna
    Lissowska, Jolanta
    Mayoral, Fermin
    Müller-Myhsok, Bertram
    Świątkowska, Beata
    Schulze, Thomas G.
    Nöthen, Markus M.
    Rietschel, Marcella
    Kelsoe, John
    Leboyer, Marion
    Jamain, Stéphane
    Etain, Bruno
    Bellivier, Frank
    Vincent, John B.
    Alda, Martin
    O'Donovan, Claire
    Cervantes, Pablo
    Biernacka, Joanna M.
    Frye, Mark
    McElroy, Susan L.
    Scott, Laura J.
    Stahl, Eli A.
    Landén, Mikael
    Hamshere, Marian L.
    Smeland, Olav B.
    Djurovic, Srdjan
    Vaaler, Arne E.
    Andreassen, Ole A.
    Baune, Bernhard T.
    Air, Tracy
    Preisig, Martin
    Uher, Rudolf
    Levinson, Douglas F.
    Weissman, Myrna M.
    Potash, James B.
    Shi, Jianxin
    Knowles, James A.
    Perlis, Roy H.
    Lucae, Susanne
    Boomsma, Dorret I
    Penninx, Brenda W. J. H.
    Hottenga, Jouke-Jan
    de Geus, Eco J. C.
    Willemsen, Gonneke
    Milaneschi, Yuri
    Tiemeier, Henning
    Grabe, Hans J.
    Teumer, Alexander
    Van der Auwera, Sandra
    Völker, Uwe
    Hamilton, Steven P.
    Magnusson, Patrik K. E.
    Viktorin, Alexander
    Mehta, Divya
    Mullins, Niamh
    Adams, Mark J.
    Breen, Gerome
    McIntosh, Andrew M.
    Lewis, Cathryn M.
    Hougaard, David M.
    Nordentoft, Merete
    Mors, Ole
    Mortensen, Preben B.
    Werge, Thomas
    Als, Thomas D.
    Børglum, Anders D.
    Petryshen, Tracey L.
    Smoller, Jordan W.
    Goldstein, Jill M.
    Sex-Dependent Shared and Nonshared Genetic Architecture Across Mood and Psychotic Disorders2022Inngår i: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 91, nr 1, s. 102-117Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND: Sex differences in incidence and/or presentation of schizophrenia (SCZ), major depressive disorder (MDD), and bipolar disorder (BIP) are pervasive. Previous evidence for shared genetic risk and sex differences in brain abnormalities across disorders suggest possible shared sex-dependent genetic risk.

    METHODS: We conducted the largest to date genome-wide genotype-by-sex (G×S) interaction of risk for these disorders using 85,735 cases (33,403 SCZ, 19,924 BIP, and 32,408 MDD) and 109,946 controls from the PGC (Psychiatric Genomics Consortium) and iPSYCH.

    RESULTS: Across disorders, genome-wide significant single nucleotide polymorphism-by-sex interaction was detected for a locus encompassing NKAIN2 (rs117780815, p = 3.2 × 10-8), which interacts with sodium/potassium-transporting ATPase (adenosine triphosphatase) enzymes, implicating neuronal excitability. Three additional loci showed evidence (p < 1 × 10-6) for cross-disorder G×S interaction (rs7302529, p = 1.6 × 10-7; rs73033497, p = 8.8 × 10-7; rs7914279, p = 6.4 × 10-7), implicating various functions. Gene-based analyses identified G×S interaction across disorders (p = 8.97 × 10-7) with transcriptional inhibitor SLTM. Most significant in SCZ was a MOCOS gene locus (rs11665282, p = 1.5 × 10-7), implicating vascular endothelial cells. Secondary analysis of the PGC-SCZ dataset detected an interaction (rs13265509, p = 1.1 × 10-7) in a locus containing IDO2, a kynurenine pathway enzyme with immunoregulatory functions implicated in SCZ, BIP, and MDD. Pathway enrichment analysis detected significant G×S interaction of genes regulating vascular endothelial growth factor receptor signaling in MDD (false discovery rate-corrected p < .05).

    CONCLUSIONS: In the largest genome-wide G×S analysis of mood and psychotic disorders to date, there was substantial genetic overlap between the sexes. However, significant sex-dependent effects were enriched for genes related to neuronal development and immune and vascular functions across and within SCZ, BIP, and MDD at the variant, gene, and pathway levels.

  • 16.
    Bodén, Robert
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Psykiatri, Akademiska sjukhuset.
    Persson, Jonas
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Psykiatri, Akademiska sjukhuset.
    Wall, Anders
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Radiologi.
    Lubberink, Mark
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Radiologi.
    Ekselius, Lisa
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Psykiatri, Akademiska sjukhuset. Uppsala Univ, Uppsala, Sweden..
    Larsson, Elna-Marie
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Radiologi.
    Antoni, Gunnar
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Farmaceutiska fakulteten, Institutionen för läkemedelskemi, Avdelningen för Molekylär Avbildning.
    Striatal Phosphodiesterase 10A and Medial Prefrontal Cortical Thickness in Patients with Schizophrenia: A PET and MRI Study2017Inngår i: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 81, nr 10, s. S386-S387Artikkel i tidsskrift (Annet vitenskapelig)
  • 17.
    Boen, Rune
    et al.
    Department of Medical Genetics, Oslo University Hospital, Oslo, Norway; Norwegian Centre for Mental Disorders Research (NORMENT), Division of Mental Health and Addiction, Oslo University Hospital and Institute of Clinical Medicine, University of Oslo, Oslo, Norway.
    Kaufmann, Tobias
    Norwegian Centre for Mental Disorders Research (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, Tübingen Center for Mental Health, University of Tübingen, Germany; German Center for Mental Health (DZPG), partner site Tübingen, Tübingen, Germany.
    van der Meer, Dennis
    Norwegian Centre for Mental Disorders Research (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.
    Frei, Oleksandr
    Norwegian Centre for Mental Disorders Research (NORMENT), Division of Mental Health and Addiction, Oslo University Hospital and Institute of Clinical Medicine, University of Oslo, Oslo, Norway; Centre for Bioinformatics, Department of Informatics, University of Oslo, Oslo, Norway.
    Agartz, Ingrid
    Norwegian Centre for Mental Disorders Research, Institute of Clinical Medicine, University of Oslo, Oslo, Norway; Department of Clinical Research, Diakonhjemmet Hospital, Oslo, Norway; Centre for Psychiatry Research, Department of Clinical Neuroscience, Karolinska Institutet and Stockholm Health Care Services, Stockholm, Sweden.
    Ames, David
    University of Melbourne Academic Unit for Psychiatry of Old Age, St George's Hospital, VIC, Kew, Australia; National Ageing Research Institute, VIC, Parkville, Australia.
    Andersson, Micael
    Umeå universitet, Medicinska fakulteten, Institutionen för integrativ medicinsk biologi (IMB). Umeå universitet, Medicinska fakulteten, Umeå centrum för funktionell hjärnavbildning (UFBI).
    Armstrong, Nicola J.
    Department of Mathematics and Statistics, Curtin University, WA, Perth, Australia.
    Artiges, Eric
    Institut National de la Santé et de la Recherche Médicale U1299, École Normale Supérieure Paris-Saclay, Université Paris Saclay, Gif-sur-Yvette, France; Établissement public de santé (EPS) Barthélemy Durand, Etampes, France.
    Atkins, Joshua R.
    School of Biomedical Sciences and Pharmacy, College of Medicine, Health and Wellbeing, University of Newcastle, NSW, Callaghan, Australia; Precision Medicine Research Program, Hunter Medical Research Institute, NSW, Newcastle, Australia; Cancer Epidemiology Unit, Nuffield Department of Population Health, University of Oxford, Oxford, United Kingdom.
    Bauer, Jochen
    University Clinic for Radiology, University of Münster, Münster, Germany.
    Benedetti, Francesco
    Psychiatry and Clinical Psychobiology Unit, Division of Neuroscience, Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS) San Raffaele Scientific Institute, Milan, Italy; Division of Neuroscience, Psychiatry and Clinical Psychobiology Unit, Istituto di Ricovero e Cura a Carattere Scientifico San Raffaele Scientific Institute, Milan, Italy.
    Boomsma, Dorret I.
    Department of Biological Psychology, Vrije Universiteit Amsterdam, Amsterdam, Netherlands.
    Brodaty, Henry
    Centre for Healthy Brain Ageing, School of Clinical Medicine, University of New South Wales, NSW, Sydney, Australia.
    Brosch, Katharina
    Department of Psychiatry and Psychotherapy, Philipps-University Marburg, Marburg, Germany.
    Buckner, Randy L.
    Department of Psychology and Center for Brain Science, Harvard University, MA, Cambridge, United States; Department of Psychiatry, Massachusetts General Hospital, MA, Boston, United States.
    Cairns, Murray J.
    School of Biomedical Sciences and Pharmacy, College of Medicine, Health and Wellbeing, University of Newcastle, NSW, Callaghan, Australia; Precision Medicine Research Program, Hunter Medical Research Institute, NSW, Newcastle, Australia.
    Calhoun, Vince
    Tri-institutional Center for Translational Research in Neuroimaging and Data Science, Georgia State University/Georgia Institute of Technology/Emory University, GA, Atlanta, United States.
    Caspers, Svenja
    Institute of Neuroscience and Medicine (INM-1), Research Centre Jülich, Jülich, Germany; Institute for Anatomy I, Medical Faculty & University Hospital Düsseldorf, Heinrich Heine University Düsseldorf, Düsseldorf, Germany.
    Cichon, Sven
    Institute of Neuroscience and Medicine (INM-1), Research Centre Jülich, Jülich, Germany; Department of Biomedicine, University of Basel, Basel, Switzerland; University Hospital Basel, Institute of Medical Genetics and Pathology, Basel, Switzerland.
    Corvin, Aiden P.
    Department of Psychiatry, Trinity College Dublin, Dublin, Ireland.
    Crespo-Facorro, Benedicto
    Instituto de Biomedicina de Sevilla, Hospital Universitario Virgen del Rocío/Centro superior de investigaciones científicas (CSIC), Sevilla, Spain; Centro de Investigación Biomédica en Red Salud Mental, Sevilla, Spain; Department of Psychiatry, University of Sevilla, Sevilla, Spain.
    Dannlowski, Udo
    Institute for Translational Psychiatry, University of Münster, Münster, Germany.
    David, Friederike S.
    Institute of Human Genetics, University of Bonn, School of Medicine and University Hospital Bonn, Bonn, Germany.
    de Geus, Eco J.C.
    Department of Biological Psychology, Vrije Universiteit Amsterdam, Amsterdam, Netherlands.
    de Zubicaray, Greig I.
    School of Psychology and Counselling, Queensland University of Technology, QLD, Brisbane, Australia.
    Desrivières, Sylvane
    Social Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, United Kingdom.
    Doherty, Joanne L.
    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
    School of Psychology and Center for Neuroimaging, Cognition and Genomics, University of Galway, Galway, Ireland.
    Ehrlich, Stefan
    Translational Developmental Neuroscience Section, Division of Psychological and Social Medicine and Developmental Neurosciences, Faculty of Medicine, Technische Universität 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; Department of Psychology, Oslo New University College, Oslo, Norway.
    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.
    Forstner, Andreas J.
    Institute of Neuroscience and Medicine (INM-1), Research Centre Jülich, Jülich, Germany; Institute of Human Genetics, University of Bonn, School of Medicine and University Hospital Bonn, Bonn, Germany.
    Fortaner-Uyà, Lidia
    Psychiatry and Clinical Psychobiology Unit, Division of Neuroscience, Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS) San Raffaele Scientific Institute, Milan, Italy; Division of Neuroscience, Psychiatry and Clinical Psychobiology Unit, Istituto di Ricovero e Cura a Carattere Scientifico San Raffaele Scientific Institute, Milan, Italy.
    Frouin, Vincent
    Neurospin, Commissariat a l'Energie Atomique (CEA), Université Paris-Saclay, Gif-sur-Yvette, France.
    Fukunaga, Masaki
    Section of Brain Function Information, National Institute for Physiological Sciences, Okazaki, Japan.
    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.
    Glahn, David C.
    Department of Psychiatry and Behavioral Sciences, Boston Children's Hospital, MA, Boston, United States; Department of Psychiatry, Harvard Medical School, MA, Boston, United States.
    Goltermann, Janik
    Institute for Translational Psychiatry, University of Münster, Münster, Germany.
    Grabe, Hans J.
    Department of Psychiatry and Psychotherapy, University Medicine Greifswald, Greifswald, Germany.
    Green, Melissa J.
    Discipline of Psychiatry and Mental Health, School of Clinical Medicine, University of New South Wales, NSW, Sydney, Australia; Neuroscience Research Australia, NSW, Sydney, Australia.
    Groenewold, Nynke A.
    Department of Psychiatry and Mental Health, Neuroscience Institute, University of Cape Town, Cape Town, South Africa.
    Grotegerd, Dominik
    Institute for Translational Psychiatry, University of Münster, Münster, Germany.
    Grøntvedt, Gøril Rolfseng
    Department of Neuromedicine and Movement Science, Faculty of Medicine and Health Sciences, Norwegian University of Science and Technology, Trondheim, Norway; Department of Neurology and Clinical Neurophysiology, University Hospital of Trondheim, Trondheim, Norway.
    Hahn, Tim
    Institute for Translational Psychiatry, University of Münster, Münster, Germany.
    Hashimoto, Ryota
    Department of Pathology of Mental Diseases, National Institute of Mental Health, National Center of Neurology and Psychiatry, Tokyo, Kodaira, Japan.
    Hehir-Kwa, Jayne Y.
    Princess Máxima Center for Pediatric Oncology, Utrecht, Netherlands.
    Henskens, Frans A.
    School of Medicine and Public Health, University of Newcastle, NSW, Newcastle, Australia; Priority Research Centre for Health Behaviour, University of Newcastle, NSW, Newcastle, Australia.
    Holmes, Avram J.
    Department of Psychiatry, Rutgers University, NJ, New Brunswick, United States; Brain Health Institute, Rutgers University, NJ, Piscataway, United States.
    Håberg, Asta K.
    Department of Neuromedicine and Movement Science, Faculty of Medicine and Health Sciences, Norwegian University of Science and Technology, Trondheim, Norway; Department of Radiology and Nuclear Medicine, St. Olav's Hospital, Trondheim, Norway.
    Haavik, Jan
    Department of Biomedicine, University of Bergen, Bergen, Norway; Division of Psychiatry, Haukeland University Hospital, Bergen, Norway.
    Jacquemont, Sebastien
    Sainte Justine Hospital Research Center, QC, Montreal, Canada; Department of Pediatrics, University of Montreal, QC, Montreal, Canada.
    Jansen, Andreas
    Department of Psychiatry and Psychotherapy, Philipps-University Marburg, Marburg, Germany; Core-Facility Brainimaging and Department of Psychiatry, Faculty of Medicine, Philipps-University Marburg, Marburg, Germany.
    Jockwitz, Christiane
    Institute of Neuroscience and Medicine (INM-1), Research Centre Jülich, Jülich, Germany; Institute for Anatomy I, Medical Faculty & University Hospital Düsseldorf, Heinrich Heine University Düsseldorf, Düsseldorf, Germany.
    Jönsson, Erik G.
    Norwegian Centre for Mental Disorders Research, Institute of Clinical Medicine, University of Oslo, Oslo, Norway; Centre for Psychiatry Research, Department of Clinical Neuroscience, Karolinska Institutet and Stockholm Health Care Services, Stockholm Region, Stockholm, Sweden.
    Kikuchi, Masataka
    Department of Genome Informatics, Graduate School of Medicine, Osaka University, Osaka, Japan; Department of Computational Biology and Medical Sciences, Graduate School of Frontier Science, The University of Tokyo, Chiba, Japan.
    Kircher, Tilo
    Department of Psychiatry and Psychotherapy, Philipps-University Marburg, Marburg, Germany.
    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, Center for Medical Genetics and Molecular Medicine, Haukeland University Hospital, Bergen, Norway.
    Leu, Costin
    Department of Clinical and Experimental Epilepsy, UCL Queen Square Institute of Neurology, University College London, London, United Kingdom; Department of Neurology, McGovern Medical School, UTHealth Houston, TX, Houston, United States.
    Linden, David E.
    Neuroscience and Mental Health Innovation Institute, Cardiff University, Cardiff, United Kingdom; School for Mental Health and Neuroscience, Department of Psychiatry and Neuropsychology, Faculty of Health, Medicine and Life Sciences, Maastricht University, Maastricht, Netherlands.
    Liu, Jingyu
    Department of Computer Science and Center for Translational Research in Neuroimaging and Data Science, Georgia State University, GA, Atlanta, United States.
    Loughnan, Robert
    Department of Cognitive Science and Population Neuroscience and Genetics Lab, University of California San Diego, CA, La Jolla, United States.
    Mather, Karen A.
    Centre for Healthy Brain Ageing, School of Clinical Medicine, University of New South Wales, NSW, Sydney, Australia.
    McMahon, Katie L.
    School of Clinical Sciences, Queensland University of Technology, QLD, Brisbane, Australia.
    McRae, Allan F.
    Institute for Molecular Bioscience, The University of Queensland, QLD, Brisbane, Australia.
    Medland, Sarah E.
    Psychiatric Genetics, Queensland Institute of Medical Research (QIMR) Berghofer Medical Research Institute, QLD, Brisbane, Australia; University of Queensland, QLD, Brisbane, Australia; Queensland University of Technology, QLD, Brisbane, Australia.
    Meinert, Susanne
    Institute for Translational Psychiatry, University of Münster, Münster, Germany; Institute for Translational Neuroscience, University of Münster, Münster, Germany.
    Moreau, Clara A.
    Imaging Genetics Center, Mark and Mary Stevens Institute for Neuroimaging and Informatics, Keck School of Medicine, University of Southern California, CA, Marina del Rey, United States.
    Morris, Derek W.
    Centre for Neuroimaging, Cognition and Genomics, School of Biological and Chemical Sciences, University of Galway, Galway, Ireland.
    Mowry, Bryan J.
    Queensland Brain Institute and Queensland Centre for Mental Health Research, University of Queensland, QLD, Brisbane, Australia.
    Mühleisen, Thomas W.
    Institute of Neuroscience and Medicine (INM-1), Research Centre Jülich, Jülich, Germany; Institute for Anatomy I, Medical Faculty & University Hospital Düsseldorf, Heinrich Heine University Düsseldorf, Düsseldorf, Germany; Department of Biomedicine, University of Basel, Basel, Switzerland.
    Nenadić, Igor
    Department of Psychiatry and Psychotherapy, Philipps-University Marburg, Marburg, Germany.
    Nöthen, Markus M.
    Institute of Human Genetics, University of Bonn, School of Medicine and University Hospital Bonn, Bonn, Germany.
    Nyberg, Lars
    Umeå universitet, Medicinska fakulteten, Institutionen för integrativ medicinsk biologi (IMB). Umeå universitet, Medicinska fakulteten, Institutionen för strålningsvetenskaper. Umeå universitet, Medicinska fakulteten, Umeå centrum för funktionell hjärnavbildning (UFBI).
    Ophoff, Roel A.
    Department of Psychiatry, Erasmus University Medical Center, Rotterdam, Netherlands; Semel Institute for Neuroscience and Human Behavior, Departments of Psychiatry and Biobehavioral Sciences and Psychology, University of California Los Angeles, CA, Los Angeles, United States.
    Owen, Michael J.
    Centre for Neuropsychiatric Genetics and Genomics, Cardiff University, Cardiff, United Kingdom; Division of Psychological Medicine and Clinical Neurosciences, Cardiff University, Cardiff, United Kingdom.
    Pantelis, Christos
    Melbourne Neuropsychiatry Centre, Department of Psychiatry, University of Melbourne, Carlton South, Victoria, Australia; Western Centre for Health Research and Education, Sunshine Hospital, VIC, St Albans, Australia.
    Paolini, Marco
    Psychiatry and Clinical Psychobiology Unit, Division of Neuroscience, Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS) San Raffaele Scientific Institute, Milan, Italy; Division of Neuroscience, Psychiatry and Clinical Psychobiology Unit, Istituto di Ricovero e Cura a Carattere Scientifico San Raffaele Scientific Institute, Milan, Italy.
    Paus, Tomas
    Departments of Psychiatry and Neuroscience, Faculty of Medicine and Sainte Justine Hospital Research Center, University of Montreal, QC, Montreal, Canada; Departments of Psychiatry and Psychology, University of Toronto, ON, Toronto, Canada.
    Pausova, Zdenka
    The Hospital for Sick Children, ON, Toronto, Canada; Department of Physiology, University of Toronto, ON, Toronto, Canada.
    Persson, Karin
    Department of Geriatric Medicine, Oslo University Hospital, Oslo, Norway; Norwegian National Centre for Ageing and Health, Vestfold Hospital Trust, Tønsberg, Norway.
    Quidé, Yann
    Neuroscience Research Australia, NSW, Sydney, Australia; School of Psychology, University of New South Wales, NSW, Sydney, Australia.
    Marques, Tiago Reis
    Psychosis Studies, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, United Kingdom.
    Sachdev, Perminder S.
    Centre for Healthy Brain Ageing, School of Clinical Medicine, University of New South Wales, NSW, Sydney, Australia; Neuropsychiatric Institute, Prince of Wales Hospital, NSW, Sydney, Australia.
    Sando, Sigrid B.
    Department of Neuromedicine and Movement Science, Faculty of Medicine and Health Sciences, Norwegian University of Science and Technology, Trondheim, Norway; Department of Neurology and Clinical Neurophysiology, University Hospital of Trondheim, Trondheim, Norway.
    Schall, Ulrich
    Hunter Medical Research Institute, NSW, Newcastle, Australia.
    Scott, Rodney J.
    School of Biomedical Sciences and Pharmacy, College of Medicine, Health and Wellbeing, University of Newcastle, NSW, Callaghan, Australia; Hunter Medical Research Institute, NSW, Newcastle, Australia; Division of Molecular Medicine, New South Wales Health Pathology, NSW, Newcastle, Australia.
    Selbæk, Geir
    Department of Geriatric Medicine, Oslo University Hospital, Oslo, Norway; Norwegian National Centre for Ageing and Health, Vestfold Hospital Trust, Tønsberg, Norway; Faculty of Medicine, University of Oslo, Oslo, Norway.
    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.
    Neuroscience and Mental Health Innovation Institute, Cardiff University, Cardiff, United Kingdom.
    Sisodiya, Sanjay M.
    Department of Clinical and Experimental Epilepsy, UCL Queen Square Institute of Neurology, University College London, London, United Kingdom; Chalfont Centre for Epilepsy, Chalfont St Peter, United Kingdom.
    Stein, Frederike
    Department of Psychiatry and Psychotherapy, Philipps-University Marburg, Marburg, Germany.
    Stein, Dan J.
    SA MRC Unit on Risk and Resilience in Mental Disorders, Department of Psychiatry and Neuroscience Institute, University of Cape Town, Cape Town, South Africa.
    Straube, Benjamin
    Department of Psychiatry and Psychotherapy, Philipps-University Marburg, Marburg, Germany.
    Streit, Fabian
    Department of Genetic Epidemiology in Psychiatry, Central Institute of Mental Health, Medical Faculty Mannheim, University of Heidelberg, Mannheim, Germany.
    Strike, Lachlan T.
    Psychiatric Genetics, Queensland Institute of Medical Research (QIMR) Berghofer Medical Research Institute, QLD, Brisbane, Australia; School of Psychology and Counselling, Faculty of Health, Queensland University of Technology, Brisbane, Australia.
    Teumer, Alexander
    Department of Psychiatry and Psychotherapy, University Medicine Greifswald, Greifswald, Germany; Institute for Community Medicine, University Medicine Greifswald, Greifswald, Germany; German Centre for Cardiovascular Research, Greifswald, Germany.
    Teutenberg, Lea
    Department of Psychiatry and Psychotherapy, Philipps-University Marburg, Marburg, Germany.
    Thalamuthu, Anbupalam
    Centre for Healthy Brain Ageing, School of Clinical Medicine, University of New South Wales, NSW, Sydney, Australia.
    Tooney, Paul A.
    School of Biomedical Sciences and Pharmacy, College of Medicine, Health and Wellbeing, University of Newcastle, NSW, Callaghan, Australia; Hunter Medical Research Institute, NSW, Newcastle, Australia.
    Tordesillas-Gutierrez, Diana
    Instituto de Física de Cantabria UC-CSIC, Santander, Spain; Department of Radiology, Marqués de Valdecilla University Hospital, Valdecilla Biomedical Research Institute, Instituto de Investigación Sanitaria Valdecilla, Santander, Spain.
    Trollor, Julian N.
    Department of Developmental Disability Neuropsychiatry and Centre for Healthy Brain Ageing, School of Clinical Medicine, University of New South Wales, NSW, Sydney, Australia.
    van ’t Ent, Dennis
    Department of Biological Psychology, Vrije Universiteit Amsterdam, Amsterdam, Netherlands.
    van den Bree, Marianne B.M.
    Institute of Psychological Medicine and Clinical Neurosciences and Centre for Neuropsychiatric Genetics and Genomics, Cardiff University, Cardiff, United Kingdom; Institute for Translational Neuroscience, University of Münster, Münster, Germany.
    van Haren, Neeltje E.M.
    Department of Child and Adolescent Psychiatry/Psychology, Erasmus University Medical Centre, Rotterdam, Netherlands; Department of Psychiatry, University Medical Centre Utrecht, Utrecht, Netherlands.
    Vázquez-Bourgon, Javier
    Centro de Investigación Biomédica en Red Salud Mental, Sevilla, Spain; Department of Psychiatry, University Hospital Maqués de Valdecilla, Instituto de Investigación Sanitaria Valdecilla, Santander, Spain; Departamento de Medicina y Psiquiatría, Universidad de Cantabria, Santander, Spain.
    Völzke, Henry
    German Centre for Cardiovascular Research, Greifswald, Germany; Greifswald University Hospital, Greifswald, Germany.
    Wen, Wei
    Centre for Healthy Brain Ageing, School of Clinical Medicine, University of New South Wales, NSW, Sydney, Australia.
    Wittfeld, Katharina
    Department of Psychiatry and Psychotherapy, University Medicine Greifswald, Greifswald, Germany.
    Ching, Christopher R.K.
    Imaging Genetics Center, Mark and Mary Stevens Institute for Neuroimaging and Informatics, Keck School of Medicine, University of Southern California, CA, Marina del Rey, United States.
    Westlye, Lars T.
    Norwegian Centre for Mental Disorders Research (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.
    Thompson, Paul M.
    Imaging Genetics Center, Mark and Mary Stevens Institute for Neuroimaging and Informatics, Keck School of Medicine, University of Southern California, CA, Marina del Rey, United States.
    Bearden, Carrie E.
    Semel Institute for Neuroscience and Human Behavior, Departments of Psychiatry and Biobehavioral Sciences and Psychology, University of California Los Angeles, CA, Los Angeles, United States.
    Selmer, Kaja K.
    Department of Research and Innovation, Division of Clinical Neuroscience, Oslo University Hospital and the University of Oslo, Oslo, Norway.
    Alnæs, Dag
    Norwegian Centre for Mental Disorders Research (NORMENT), Division of Mental Health and Addiction, Oslo University Hospital and Institute of Clinical Medicine, University of Oslo, Oslo, Norway; Kristiania University College, Oslo, Norway.
    Andreassen, Ole A.
    Norwegian Centre for Mental Disorders Research (NORMENT), Division of Mental Health and Addiction, Oslo University Hospital and Institute of Clinical Medicine, University of Oslo, Oslo, Norway; Norwegian Centre for Mental Disorders Research, Institute of Clinical Medicine, University of Oslo, Oslo, Norway; KG Jebsen Centre for Neurodevelopmental Disorders, University of Oslo, Oslo, Norway.
    Sønderby, Ida E.
    Department of Medical Genetics, Oslo University Hospital, Oslo, Norway; Norwegian Centre for Mental Disorders Research (NORMENT), Division of Mental Health and Addiction, Oslo University Hospital and Institute of Clinical Medicine, University of Oslo, Oslo, Norway; KG Jebsen Centre for Neurodevelopmental Disorders, University of Oslo, Oslo, Norway.
    Beyond the global brain differences: intraindividual variability differences in 1q21.1 distal and 15q11.2 bp1-bp2 deletion carriers2024Inngår i: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 95, nr 2, s. 147-160Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: Carriers of the 1q21.1 distal and 15q11.2 BP1-BP2 copy number variants exhibit regional and global brain differences compared with noncarriers. However, interpreting regional differences is challenging if a global difference drives the regional brain differences. Intraindividual variability measures can be used to test for regional differences beyond global differences in brain structure.

    Methods: Magnetic resonance imaging data were used to obtain regional brain values for 1q21.1 distal deletion (n = 30) and duplication (n = 27) and 15q11.2 BP1-BP2 deletion (n = 170) and duplication (n = 243) carriers and matched noncarriers (n = 2350). Regional intra-deviation scores, i.e., the standardized difference between an individual's regional difference and global difference, were used to test for regional differences that diverge from the global difference.

    Results: For the 1q21.1 distal deletion carriers, cortical surface area for regions in the medial visual cortex, posterior cingulate, and temporal pole differed less and regions in the prefrontal and superior temporal cortex differed more than the global difference in cortical surface area. For the 15q11.2 BP1-BP2 deletion carriers, cortical thickness in regions in the medial visual cortex, auditory cortex, and temporal pole differed less and the prefrontal and somatosensory cortex differed more than the global difference in cortical thickness.

    Conclusions: We find evidence for regional effects beyond differences in global brain measures in 1q21.1 distal and 15q11.2 BP1-BP2 copy number variants. The results provide new insight into brain profiling of the 1q21.1 distal and 15q11.2 BP1-BP2 copy number variants, with the potential to increase understanding of the mechanisms involved in altered neurodevelopment.

    Fulltekst (pdf)
    fulltext
  • 18.
    Brander, Gustaf
    et al.
    Karolinska Institutet, Stockholm, Sweden.
    Kuja-Halkola, Ralf
    Karolinska Institutet, Stockholm, Sweden.
    Rosenqvist, Mina
    Karolinska Institutet, Stockholm, Sweden.
    Rück, Christian
    Karolinska Institutet, Stockholm, Sweden.
    Serlachius, Eva
    Karolinska Institutet, Stockholm, Sweden.
    Larsson, Henrik
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Mataix-Cols, David
    Karolinska Institutet, Stockholm, Sweden.
    Is Tic-Related OCD a Familial Subtype of the Disorder?: A Swedish Population Cohort Study2019Inngår i: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 85, nr 10, s. S221-S221Artikkel i tidsskrift (Annet vitenskapelig)
  • 19. Brazel, David M.
    et al.
    Jiang, Yu
    Hughey, Jordan M.
    Turcot, Valérie
    Zhan, Xiaowei
    Gong, Jian
    Batini, Chiara
    Weissenkampen, J. Dylan
    Liu, MengZhen
    Barnes, Daniel R.
    Bertelsen, Sarah
    Chou, Yi-Ling
    Erzurumluoglu, A. Mesut
    Faul, Jessica D.
    Haessler, Jeff
    Hammerschlag, Anke R.
    Hsu, Chris
    Kapoor, Manav
    Lai, Dongbing
    Le, Nhung
    de Leeuw, Christiaan A.
    Loukola, Anu
    Mangino, Massimo
    Melbourne, Carl A.
    Pistis, Giorgio
    Qaiser, Beenish
    Rohde, Rebecca
    Shao, Yaming
    Stringham, Heather
    Wetherill, Leah
    Zhao, Wei
    Agrawal, Arpana
    Bierut, Laura
    Chen, Chu
    Eaton, Charles B.
    Goate, Alison
    Haiman, Christopher
    Heath, Andrew
    Iacono, William G.
    Martin, Nicholas G.
    Polderman, Tinca J.
    Reiner, Alex
    Rice, John
    Schlessinger, David
    Scholte, H. Steven
    Smith, Jennifer A.
    Tardif, Jean-Claude
    Tindle, Hilary A.
    van der Leij, Andries R.
    Boehnke, Michael
    Chang-Claude, Jenny
    Cucca, Francesco
    David, Sean P.
    Foroud, Tatiana
    Howson, Joanna M. M.
    Kardia, Sharon L. R.
    Kooperberg, Charles
    Laakso, Markku
    Lettre, Guillaume
    Madden, Pamela
    McGue, Matt
    North, Kari
    Posthuma, Danielle
    Spector, Timothy
    Stram, Daniel
    Tobin, Martin D.
    Weir, David R.
    Kaprio, Jaakko
    Abecasis, Gonçalo R.
    Liu, Dajiang J.
    Vrieze, Scott
    Franks, Paul W. ()
    Exome Chip Meta-analysis Fine Maps Causal Variants and Elucidates the Genetic Architecture of Rare Coding Variants in Smoking and Alcohol Use2019Inngår i: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 85, nr 11, s. 946-955Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND: Smoking and alcohol use have been associated with common genetic variants in multiple loci. Rare variants within these loci hold promise in the identification of biological mechanisms in substance use. Exome arrays and genotype imputation can now efficiently genotype rare nonsynonymous and loss of function variants. Such variants are expected to have deleterious functional consequences and to contribute to disease risk.

    METHODS: We analyzed ∼250,000 rare variants from 16 independent studies genotyped with exome arrays and augmented this dataset with imputed data from the UK Biobank. Associations were tested for five phenotypes: cigarettes per day, pack-years, smoking initiation, age of smoking initiation, and alcoholic drinks per week. We conducted stratified heritability analyses, single-variant tests, and gene-based burden tests of nonsynonymous/loss-of-function coding variants. We performed a novel fine-mapping analysis to winnow the number of putative causal variants within associated loci.

    RESULTS: Meta-analytic sample sizes ranged from 152,348 to 433,216, depending on the phenotype. Rare coding variation explained 1.1% to 2.2% of phenotypic variance, reflecting 11% to 18% of the total single nucleotide polymorphism heritability of these phenotypes. We identified 171 genome-wide associated loci across all phenotypes. Fine mapping identified putative causal variants with double base-pair resolution at 24 of these loci, and between three and 10 variants for 65 loci. Twenty loci contained rare coding variants in the 95% credible intervals.

    CONCLUSIONS: Rare coding variation significantly contributes to the heritability of smoking and alcohol use. Fine-mapping genome-wide association study loci identifies specific variants contributing to the biological etiology of substance use behavior.

  • 20.
    Brikell, Isabell
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Ghirardi, Laura
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    D'Onofrio, Brian M.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Psychological and Brain Sciences, Indiana University, Bloomington, United States.
    Dunn, David W.
    Department of Psychiatry, Riley Child and Adolescent Psychiatry Clinic, Indiana University School of Medicine, Indiana University Health Physicians, Indianapolis Indiana, United States.
    Almqvist, Catarina
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Astrid Lindgren Children's Hospital, Karolinska University Hospital, Stockholm, Sweden.
    Dalsgaard, Søren
    National Centre for Register-Based Research, Department of Economics, Aarhus University, Aarhus, Denmark; The Lundbeck Foundation Initiative for Integrative Psychiatric Research, Aarhus University, Aarhus, Denmark; Department for Child and Adolescent Psychiatry, Hospital of Telemark, Kragerø, Norway.
    Kuja-Halkola, Ralf
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Larsson, Henrik
    Örebro universitet, Institutionen för medicinska vetenskaper. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Familial Liability to Epilepsy and Attention-Deficit/Hyperactivity Disorder: A Nationwide Cohort Study2018Inngår i: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 83, nr 2, s. 173-180Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND: Epilepsy and attention-deficit/hyperactivity disorder (ADHD) are strongly associated; however, the underlying factors contributing to their co-occurrence remain unclear. A shared genetic liability has been proposed as one possible mechanism. Therefore, our goal in this study was to investigate the familial coaggregation of epilepsy and ADHD and to estimate the contribution of genetic and environmental risk factors to their co-occurrence.

    METHODS: We identified 1,899,654 individuals born between 1987 and 2006 via national Swedish registers and linked each individual to his or her biological relatives. We used logistic regression to estimate the association between epilepsy and ADHD within individual and across relatives. Quantitative genetic modeling was used to decompose the cross-disorder covariance into genetic and environmental factors.

    RESULTS: Individuals with epilepsy had a statistically significant increased risk of ADHD (odds ratio [OR] = 3.47, 95% confidence interval [CI] = 3.33-3.62). This risk increase extended to children whose mothers had epilepsy (OR = 1.85, 95% CI = 1.75-1.96), children whose fathers had epilepsy (OR = 1.64, 95% CI = 1.54-1.74), full siblings (OR = 1.56, 95% CI = 1.46-1.67), maternal half siblings (OR = 1.28, 95% CI = 1.14-1.43), paternal half siblings (OR = 1.10, 95% CI = 0.96-1.25), and cousins (OR = 1.15, 95% CI = 1.10-1.20). The genetic correlation was 0.21 (95% CI = 0.02-0.40) and explained 40% of the phenotypic correlation between epilepsy and ADHD, with the remaining variance largely explained by nonshared environmental factors (49%, nonshared environmental correlation = 0.36, 95% CI = 0.23-0.49). The contribution of shared environmental factors to the cross-disorder overlap was not statistically significant (11%, shared environmental correlation = 0.32, 95% CI = 20.16-0.79).

    CONCLUSIONS: This study demonstrates a strong and etiologically complex association between epilepsy and ADHD, with shared familial factors and risk factors unique to the individual contributing to co-occurrence of the disorders. Our findings suggest that epilepsy and ADHD may share less genetic risk as compared with other neurodevelopmental disorders.

  • 21.
    Browning, Michael
    et al.
    Univ Oxford, Dept Psychiat, Oxford OX1 2JD, England.
    Holmes, Emily A.
    Univ Oxford, Dept Psychiat, Oxford OX1 2JD, England.
    Charles, Matthew
    UCL, Res Dept Clin Educ & Hlth Psychol, London WC1E 6BT, England.
    Cowen, Philip J.
    Univ Oxford, Dept Psychiat, Oxford OX1 2JD, England.
    Harmer, Catherine J.
    Univ Oxford, Dept Psychiat, Oxford OX1 2JD, England.
    Using Attentional Bias Modification as a Cognitive Vaccine Against Depression2012Inngår i: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 72, nr 7, s. 572-579Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: Negative attentional biases are thought to increase the risk of recurrence in depression, suggesting that reduction of such biases may be a plausible strategy in the secondary prevention of the illness. However, no previous study has tested whether reducing negative attentional bias causally affects risk factors for depressive recurrence. The current experimental medicine study reports the effects of a computerized attentional bias modification (ABM) procedure on intermediate measures of the risk of depressive recurrence (residual depressive symptoms and the cortisol awakening response) in patients with recurrent depression. Methods: Sixty-one patients with at least two previous episodes of depression who were currently in remission were randomized to receive either an active (positive) or placebo computer-based ABM regime. The ABM regime presented either pictures of faces or words. Residual depressive symptoms, measured using the Beck Depression Inventory and the cortisol awakening response were measured immediately before and after completion of the bias modification and then again after 4 weeks' follow-up. Results: Positive, face-based ABM reduced both measures of recurrence risk (Beck Depression Inventory and cortisol awakening response). This effect occurred during the month following completion of bias modification. Word-based modification did not influence the outcome measures. Conclusions: Positive face-based ABM was able to reduce intermediate measures of recurrence risk in previously depressed patients. These results suggest that ABM may provide a "cognitive vaccine" against depression and offer a useful strategy in the secondary prevention of the illness.

  • 22.
    Browning, Michael
    et al.
    Univ Oxford, Warneford Hosp, Dept Psychiat, Oxford OX3 7JX, England.
    Holmes, Emily A.
    Univ Oxford, Warneford Hosp, Dept Psychiat, Oxford OX3 7JX, England.
    Murphy, Susannah E.
    Univ Oxford, Warneford Hosp, Dept Psychiat, Oxford OX3 7JX, England.
    Goodwin, Guy M.
    Univ Oxford, Warneford Hosp, Dept Psychiat, Oxford OX3 7JX, England.
    Harmer, Catherine J.
    Univ Oxford, Warneford Hosp, Dept Psychiat, Oxford OX3 7JX, England.
    Lateral Prefrontal Cortex Mediates the Cognitive Modification of Attentional Bias2010Inngår i: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 67, nr 10, s. 919-925Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: A tendency to orient attention toward threatening stimuli may be involved in the etiology of anxiety disorders. In keeping with this, both psychological and pharmacological treatments of anxiety reduce this negative attentional bias. It has been hypothesized, but not proved, that psychological interventions may alter the function of prefrontal regions supervising the allocation of attentional resources. Methods: The current study examined the effects of a cognitive training regime on attention. Participants were randomly assigned to one of two training conditions: "attend-threat" training, which increases negative attentional bias, or "avoid-threat" training, which reduces it. The behavioral effects of training were assessed using a sample of 24 healthy participants. Functional magnetic resonance imaging data were collected in a further 29 healthy volunteers using a protocol that allowed the influence of both stimuli valence and attention to be discriminated. Results: Cognitive training induced the expected attentional biases in healthy volunteers. Further, the training altered lateral frontal activation to emotional stimuli, with these areas responding specifically to violations of the behavioral rules learned during training. Connectivity analysis confirmed that the identified lateral frontal regions were influencing attention as indexed by activity in visual association cortex. Conclusions: Our results indicate that frontal control over the processing of emotional stimuli may be tuned by psychological interventions in a manner predicted to regulate levels of anxiety. This directly supports the proposal that psychological interventions may influence attention via an effect on the prefrontal cortex.

  • 23.
    Castensson, Anja
    et al.
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Biologiska sektionen, Institutionen för evolutionsbiologi, Evolutionsbiologi.
    Emilsson, Lina
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Biologiska sektionen, Institutionen för evolution, genomik och systematik, Evolutionsbiologi.
    Sundberg, Rolf
    Jazin, Elena
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Biologiska sektionen, Institutionen för evolution, genomik och systematik, Evolutionsbiologi.
    Decrease of serotonin receptor 2C in schizophrenia brains identified by high-resolution mRNA expression analysis2003Inngår i: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 54, nr 11, s. 1212-1221Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND: RNA expression profiling can provide hints for the selection of candidate susceptibility genes, for formulation of hypotheses about the development of a disease, and/or for selection of candidate gene targets for novel drug development. We measured messenger RNA expression levels of 16 candidate genes in brain samples from 55 schizophrenia patients and 55 controls. This is the largest sample so far used to identify genes differentially expressed in schizophrenia brains. METHODS: We used a sensitive real-time polymerase chain reaction methodology and a novel statistical approach, including the development of a linear model of analysis of covariance type. RESULTS: We found two genes differentially expressed: monoamine oxidase B was significantly increased in schizophrenia brain (p =.001), whereas one of the serotonin receptor genes, serotonin receptor 2C, was significantly decreased (p =.001). Other genes, previously proposed to be differentially expressed in schizophrenia brain, were invariant in our analysis. CONCLUSIONS:The differential expression of serotonin receptor 2C is particularly relevant for the development of new atypical antipsychotic drugs. The strategy presented here is useful to evaluate hypothesizes for the development of the disease proposed by other investigators.

  • 24.
    Castensson, Anja
    et al.
    Uppsala University, Sweden.
    Emilsson, Lina
    Uppsala University, Sweden.
    Sundberg, Rolf
    Stockholms universitet, Naturvetenskapliga fakulteten, Matematiska institutionen.
    Jazin, Elena
    Uppsala University, Sweden.
    Decrease of serotonin receptor 2C in schizophrenia brains identified by high-resolution mRNA expression analysis2003Inngår i: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 54, nr 11, s. 1212-1221Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: RNA expression profiling can provide hints for the selection of candidate susceptibility genes, for formulation of hypotheses about the development of a disease, and/or for selection of candidate gene targets for novel drug development. We measured messenger RNA expression levels of 16 candidate genes in brain samples from 55 schizophrenia patients and 55 controls. This is the largest sample so far used to identify genes differentially expressed in schizophrenia brains.

    Methods: We used a sensitive real-time polymerase chain reaction methodology and a novel statistical approach, including the development of a linear model of analysis of covariance type.

    Results: We found two genes differentially expressed: monoamine oxidase B was significantly increased in schizophrenia brain (p = .001), whereas one of the serotonin receptor genes, serotonin receptor 2C, was significantly decreased (p = .001). Other genes, previously proposed to be differentially expressed in schizophrenia brain, were invariant in our analysis.

    Conclusions: The differential expression of serotonin receptor 2C is particularly relevant for the development of new atypical antipsychotic drugs. The strategy presented here is useful to evaluate hypothesizes for the development of the disease proposed by other investigators.

  • 25.
    Chang, Zheng
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    D'Onofrio, Brian M.
    Department of Psychological and Brain Sciences, Indiana University, Bloomington, USA.
    Quinn, Patrick D.
    Department of Psychological and Brain Sciences, Indiana University, Bloomington, USA.
    Lichtenstein, Paul
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Larsson, Henrik
    Örebro universitet, Institutionen för medicinska vetenskaper. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Medication for Attention-Deficit/Hyperactivity Disorder and Risk for Depression: A Nationwide Longitudinal Cohort Study2016Inngår i: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 80, nr 12, s. 916-922Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: Attention-deficit/hyperactivity disorder (ADHD) is associated with high rates of psychiatric comorbidity, including depression. However, it is unclear whether ADHD medication increases or decreases the risk for depression.

    Methods: We studied all individuals with a diagnosis of ADHD born between 1960 and 1998 in Sweden (N = 38,752). We obtained data for prescription of ADHD medication, diagnosis of depression and other psychiatric disorders, and sociodemographic factors from population-based registers. The association between ADHD medication and depression was estimated with Cox proportional hazards regression.

    Results: After adjustment for sociodemographic and clinical confounders, ADHD medication was associated with a reduced long-term risk (i.e., 3 years later) for depression (hazard ratio = 0.58; 95% confidence interval, 0.51-0.67). The risk was lower for longer duration of ADHD medication. Also, ADHD medication was associated with reduced rates of concurrent depression; within-individual analysis suggested that occurrence of depression was 20% less common during periods when patients received ADHD medication compared with periods when they did not (hazard ratio = 0.80; 95% confidence interval, 0.70-0.92).

    Conclusions Our study suggests that ADHD medication does not increase the risk of later depression; rather, medication was associated with a reduced risk for subsequent and concurrent depression.

  • 26.
    Chang, Zheng
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Ghirardi, Laura
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Quinn, Patrick D.
    Department of Applied Health Science, School of Public Health, Bloomington Indiana, USA.
    Asherson, Philip
    Social Genetic and Developmental Psychiatry, Institute of Psychiatry, Psychology and Neuroscience, King’s College London, London, United Kingdom.
    D'Onofrio, Brian M.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Psychological and Brain Sciences, Indiana University, Bloomington Indiana, USA.
    Larsson, Henrik
    Örebro universitet, Institutionen för medicinska vetenskaper. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Risks and Benefits of Attention-Deficit/Hyperactivity Disorder Medication on Behavioral and Neuropsychiatric Outcomes: A Qualitative Review of Pharmacoepidemiology Studies Using Linked Prescription Databases2019Inngår i: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 86, nr 5, s. 335-343Artikkel, forskningsoversikt (Fagfellevurdert)
    Abstract [en]

    Attention-deficit/hyperactivity disorder (ADHD) medication is one of the most commonly prescribed medication classes in child and adolescent psychiatry, and its use is increasing rapidly in adult psychiatry. However, major questions and concerns remain regarding the benefits and risks of ADHD medication, especially in real-world settings. We conducted a qualitative systematic review of studies that investigated the effects of ADHD medication on behavioral and neuropsychiatric outcomes using linked prescription databases from the last 10 years and identified 40 studies from Europe, North America, and Asia. Among them, 18 used within-individual designs to account for confounding by indication. These studies suggested short-term beneficial effects of ADHD medication on several behavioral or neuropsychiatric outcomes (i.e., injuries, motor vehicle accidents, education, substance use disorder), with estimates suggesting relative risk reduction of 9% to 58% for these outcomes. The within-individual studies found no evidence of increased risks for suicidality and seizures. Replication studies are needed for several other important outcomes (i.e., criminality, depression, mania, psychosis). The available evidence from pharmacoepidemiology studies on long-term effects of ADHD medication was less clear. We discuss time-varying confounding and other limitations that should be considered when interpreting results from pharmacoepidemiology studies. Furthermore, we highlight several knowledge gaps to be addressed in future research and implications for research on mechanisms of outcomes of ADHD medications.

  • 27.
    Chang, Zheng
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Quinn, Patrick D.
    Department of Applied Health Science, School of Public Health, Indiana University, Bloomington, Indiana, USA.
    O'Reilly, Lauren
    Department of Psychological and Brain Sciences, Indiana University, Bloomington, Indiana, USA.
    Sjölander, Arvid
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Hur, Kwan
    Center for Health Statistics, University of Chicago, Chicago, Illinois, USA.
    Gibbons, Robert
    Center for Health Statistics, University of Chicago, Chicago, Illinois, USA.
    Larsson, Henrik
    Örebro universitet, Institutionen för medicinska vetenskaper.
    D'Onofrio, Brian M.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Psychological and Brain Sciences, Indiana University, Bloomington, Indiana, USA.
    Medication for Attention-Deficit/Hyperactivity Disorder and Risk for Suicide Attempts2020Inngår i: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 88, nr 6, s. 452-458Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND: Attention-deficit/hyperactivity disorder (ADHD) is a risk factor for suicidal behavior, but the effect of ADHD medication on suicidal behavior remains unclear. This study aimed to examine the associations between medication treatment for ADHD and risk of suicide attempts.

    METHODS: We identified a large cohort of patients with ADHD (N = 3,874,728, 47.8% female patients) using data from commercial health care claims from 2005 to 2014 in the United States. We used population-level and within-individual analyses to compare risk of suicide attempts during months when individuals received prescribed stimulant or nonstimulant medication relative to months when they did not receive medication.

    RESULTS: In both population-level and within-individual analyses, ADHD medication was associated with lower odds of suicide attempts (odds ratio [OR], 0.69; 95% confidence interval [CI], 0.66-0.73; and OR, 0.61; 95% CI, 0.57-0.66, respectively). Similar reductions were found in children to middle-aged adults and in clinically relevant subgroups, including patients with ADHD with preexisting depression or substance use disorder. The reduction was mainly seen for stimulant medication (OR, 0.72; 95% CI, 0.66-0.77); nonstimulant medication was not associated with statistically significant changes in risk of suicide attempts (OR, 0.94; 95% CI, 0.74-1.19). Sensitivity analyses assessing the influence of different exposure definitions, different outcome definitions, subsets of the cohort, and different analytic approaches provided comparable results.

    CONCLUSIONS: Stimulant medication was associated with a reduced risk of suicide attempts in patients with ADHD, and nonstimulant medication is unlikely to increase the risk of suicide attempts.

  • 28.
    Cippitelli, Andrea
    et al.
    National Institute on Alcohol Abuse and Alcoholism, NIH; Bethesda, MD, USA.
    Damadzic, Ruslan
    National Institute on Alcohol Abuse and Alcoholism, NIH; Bethesda, MD, USA.
    Frankola, Kate
    National Institute on Alcohol Abuse and Alcoholism, NIH; Bethesda, MD, USA.
    Goldstein, Andrea
    National Institute on Alcohol Abuse and Alcoholism, NIH; Bethesda, MD, USA.
    Thorsell, Annika
    National Institute on Alcohol Abuse and Alcoholism, NIH; Bethesda, MD, USA.
    Singley, Erick
    National Institute on Alcohol Abuse and Alcoholism, NIH; Bethesda, MD, USA.
    Eskay, Robert L
    National Institute on Alcohol Abuse and Alcoholism, NIH; Bethesda, MD, USA.
    Heilig, Markus
    National Institute on Alcohol Abuse and Alcoholism, NIH; Bethesda, MD, USA.
    Alcohol-induced neurodegeneration, suppression of transforming growth factor-beta, and cognitive impairment in rats: prevention by group II metabotropic glutamate receptor activation2010Inngår i: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 67, nr 9, s. 823-830Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND: Glutamatergic neurotransmission has been implicated in mechanisms of alcohol-induced neurodegeneration and cognitive impairment, but the underlying mechanism remains unknown. Here, we examined whether the group II metabotropic glutamate receptor agonist LY379268 prevents neuronal death and learning deficits in a rat model of binge-like exposure to alcohol.

    METHODS: Following 4-day binge alcohol exposure concurrent with LY379268 or vehicle treatment, Fluoro-Jade B and transforming growth factor-beta (TGF-beta) staining were carried out, and reversal learning in the Morris water maze was assessed.

    RESULTS: Fluoro-Jade B staining indicating neurodegeneration was most extensive in the ventral hippocampus and the entorhinal cortex (EC). LY379268 was potently neuroprotective in the EC but not in the dentate gyrus of the hippocampus. In parallel, binge alcohol exposure suppressed TGF-beta expression in both the EC and dentate gyrus, whereas LY379268 increased TGF-beta in the EC only. Finally, neuroprotective effects of LY379268 were accompanied by prevention of deficits in spatial reversal learning.

    CONCLUSIONS: Our data support a neuroprotective role for group II metabotropic glutamate receptor agonists and TGF-beta in alcohol-induced neurodegeneration.

  • 29. Darki, Fahimeh
    et al.
    Peyrard-Janvid, Myriam
    Matsson, Hans
    Kere, Juha
    Klingberg, Torkel
    Three dyslexia susceptibility genes, DYX1C1, DCDC2, and KIAA0319, affect temporo-parietal white matter structure.2012Inngår i: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 72, nr 8, s. 671-6, artikkel-id S0006-3223(12)00445-3Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND: Volume and integrity of white matter correlate with reading ability, but the underlying factors contributing to this variability are unknown.

    METHODS: We investigated single nucleotide polymorphisms in three genes previously associated with dyslexia and implicated in neuronal migration (DYX1C1, DCDC2, KIAA0319) and white matter volume in a cohort of 76 children and young adults from the general population.

    RESULTS: We found that all three genes contained polymorphisms that were significantly associated with white matter volume in the left temporo-parietal region and that white matter volume influenced reading ability.

    CONCLUSIONS: The identified region contained white matter pathways connecting the middle temporal gyrus with the inferior parietal lobe. The finding links previous neuroimaging and genetic results and proposes a mechanism underlying variability in reading ability in both normal and impaired readers.

  • 30. de Zwarte, Sonja M. C.
    et al.
    Brouwer, Rachel M.
    Agartz, Ingrid
    Alda, Martin
    Aleman, André
    Alpert, Kathryn I.
    Bearden, Carrie E.
    Bertolino, Alessandro
    Bois, Catherine
    Bonvino, Aurora
    Bramon, Elvira
    Buimer, Elizabeth E. L.
    Cahn, Wiepke
    Cannon, Dara M.
    Cannon, Tyrone D.
    Caseras, Xavier
    Castro-Fornieles, Josefina
    Chen, Qiang
    Chung, Yoonho
    De la Serna, Elena
    Di Giorgio, Annabella
    Doucet, Gaelle E.
    Eker, Mehmet Cagdas
    Erk, Susanne
    Fears, Scott C.
    Foley, Sonya F.
    Frangou, Sophia
    Frankland, Andrew
    Fullerton, Janice M.
    Glahn, David C.
    Goghari, Vina M.
    Goldman, Aaron L.
    Gonul, Ali Saffet
    Gruber, Oliver
    de Haan, Lieuwe
    Hajek, Tomas
    Hawkins, Emma L.
    Heinz, Andreas
    Hillegers, Manon H. J.
    Hulshoff Pol, Hilleke E.
    Hultman, Christina M.
    Ingvar, Martin
    Johansson, Viktoria
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Jönsson, Erik G.
    Kane, Fergus
    Kempton, Matthew J.
    Koenis, Marinka M. G.
    Kopecek, Miloslav
    Krabbendam, Lydia
    Krämer, Bernd
    Lawrie, Stephen M.
    Lenroot, Rhoshel K.
    Marcelis, Machteld
    Marsman, Jan-Bernard C.
    Mattay, Venkata S.
    McDonald, Colm
    Meyer-Lindenberg, Andreas
    Michielse, Stijn
    Mitchell, Philip B.
    Moreno, Dolores
    Murray, Robin M.
    Mwangi, Benson
    Najt, Pablo
    Neilson, Emma
    Newport, Jason
    van Os, Jim
    Overs, Bronwyn
    Ozerdem, Aysegul
    Picchioni, Marco M.
    Richter, Anja
    Roberts, Gloria
    Aydogan, Aybala Saricicek
    Schofield, Peter R.
    Simsek, Fatma
    Soares, Jair C.
    Sugranyes, Gisela
    Toulopoulou, Timothea
    Tronchin, Giulia
    Walter, Henrik
    Wang, Lei
    Weinberger, Daniel R.
    Whalley, Heather C.
    Yalin, Nefize
    Andreassen, Ole A.
    Ching, Christopher R. K.
    van Erp, Theo G. M.
    Turner, Jessica A.
    Jahanshad, Neda
    Thompson, Paul M.
    Kahn, René S.
    van Haren, Neeltje E. M.
    The association between familial risk and brain abnormalities is disease specific: an ENIGMA-relatives study of schizophrenia and bipolar disorder2019Inngår i: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 86, nr 7, s. 545-556Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND: Schizophrenia and bipolar disorder share genetic liability, and some structural brain abnormalities are common to both conditions. First-degree relatives of patients with schizophrenia (FDRs-SZ) show similar brain abnormalities to patients, albeit with smaller effect sizes. Imaging findings in first-degree relatives of patients with bipolar disorder (FDRs-BD) have been inconsistent in the past, but recent studies report regionally greater volumes compared with control subjects.

    METHODS: We performed a meta-analysis of global and subcortical brain measures of 6008 individuals (1228 FDRs-SZ, 852 FDRs-BD, 2246 control subjects, 1016 patients with schizophrenia, 666 patients with bipolar disorder) from 34 schizophrenia and/or bipolar disorder family cohorts with standardized methods. Analyses were repeated with a correction for intracranial volume (ICV) and for the presence of any psychopathology in the relatives and control subjects.

    RESULTS: FDRs-BD had significantly larger ICV (d = +0.16, q < .05 corrected), whereas FDRs-SZ showed smaller thalamic volumes than control subjects (d = -0.12, q < .05 corrected). ICV explained the enlargements in the brain measures in FDRs-BD. In FDRs-SZ, after correction for ICV, total brain, cortical gray matter, cerebral white matter, cerebellar gray and white matter, and thalamus volumes were significantly smaller; the cortex was thinner (d < -0.09, q < .05 corrected); and third ventricle was larger (d = +0.15, q < .05 corrected). The findings were not explained by psychopathology in the relatives or control subjects.

    CONCLUSIONS: Despite shared genetic liability, FDRs-SZ and FDRs-BD show a differential pattern of structural brain abnormalities, specifically a divergent effect in ICV. This may imply that the neurodevelopmental trajectories leading to brain anomalies in schizophrenia or bipolar disorder are distinct.

    Fulltekst (pdf)
    fulltext
  • 31.
    Dickens, Alex M.
    et al.
    Turku Bioscience Center, University of Turku and Åbo Akademi University, Turku, Finland.
    Sen, Partho
    Turku Bioscience Center, University of Turku and Åbo Akademi University, Turku, Finland.
    Kempton, Matthew J.
    Department of Psychosis Studies, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, United Kingdom.
    Barrantes-Vidal, Neus
    Departament de Psicologia Clínica i de la Salut, Universitat Autònoma de Barcelona, Fundació Sanitària Sant Pere Claver, Spanish Mental Health Research Network, Barcelona, Spain.
    Iyegbe, Conrad
    Department of Psychosis Studies, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, United Kingdom.
    Nordentoft, Merete
    Mental Health Center Copenhagen and Center for Clinical Intervention and Neuropsychiatric Schizophrenia Research, Mental Health Center Glostrup, Mental Health Services in the Capital Region of Copenhagen, University of Copenhagen, Glostrup, Denmark.
    Pollak, Thomas
    Department of Psychosis Studies, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, United Kingdom.
    Riecher-Rössler, Anita
    University Psychiatric Hospital, Basel, Switzerland.
    Ruhrmann, Stephan
    Department of Psychiatry and Psychotherapy, University of Cologne, Cologne, Germany.
    Sachs, Gabriele
    Department of Psychiatry and Psychotherapy, Medical University of Vienna, Vienna, Austria.
    Bressan, Rodrigo
    Lab Interdisciplinar Neurociências Clínicas, Departimento Psiquiatria, Escola Paulista de Medicina, Universidade Federal de São Paulo, São Paulo, Brazil.
    Krebs, Marie-Odile
    University of Paris, Groupe Hospitalier Universitaire Paris Sainte-Anne, Centre d'Évaluation Pour Jeunes Adultes et Adolescents, Institut National de la Santé et de la Recherche Médicale, Institut de Psychiatrie, Paris, France.
    Amminger, G. Paul
    Centre for Youth Mental Health, University of Melbourne, Parkville, Victoria, Australia.
    de Haan, Lieuwe
    Department of Psychiatry, Amsterdam University Medical Center, Faculty of Behavioural and Movement Sciences, Vrije Universiteit, Amsterdam, The Netherlands.
    van der Gaag, Mark
    Department of Clinical Psychology and EMGO+ Institute for Health and Care Research, Faculty of Behavioural and Movement Sciences, Vrije Universiteit, Amsterdam, The Netherlands; Department of Psychosis Research, Parnassia Psychiatric Institute, The Hague, The Netherlands.
    Valmaggia, Lucia
    Department of Psychosis Studies, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, United Kingdom.
    Hyötyläinen, Tuulia
    Örebro universitet, Institutionen för naturvetenskap och teknik.
    Oresic, Matej
    Örebro universitet, Institutionen för medicinska vetenskaper. Turku Bioscience Center, University of Turku and Åbo Akademi University, Turku, Finland.
    McGuire, Philip
    Department of Psychosis Studies, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, United Kingdom.
    Dysregulated Lipid Metabolism Precedes Onset of Psychosis2021Inngår i: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 89, nr 3, s. 288-297Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND: A key clinical challenge in the management of individuals at clinical high risk for psychosis (CHR) is that it is difficult to predict their future clinical outcomes. Here, we investigated if the levels of circulating molecular lipids are related to adverse clinical outcomes in this group.

    METHODS: Serum lipidomic analysis was performed in 263 CHR individuals and 51 healthy control subjects, who were then clinically monitored for up to 5 years. Machine learning was used to identify lipid profiles that discriminated between CHR and control subjects, and between subgroups of CHR subjects with distinct clinical outcomes.

    RESULTS: At baseline, compared with control subjects, CHR subjects (independent of outcome) had higher levels of triacylglycerols with a low acyl carbon number and a double bond count, as well as higher levels of lipids in general. CHR subjects who subsequently developed psychosis (n = 50) were distinguished from those that did not (n = 213) on the basis of lipid profile at baseline using a model with an area under the receiver operating curve of 0.81 (95% confidence interval = 0.69-0.93). CHR subjects who became psychotic had lower levels of ether phospholipids than CHR individuals who did not (p < .01).

    CONCLUSIONS: Collectively, these data suggest that lipidomic abnormalities predate the onset of psychosis and that blood lipidomic measures may be useful in predicting which CHR individuals are most likely to develop psychosis.

  • 32. Dumontheil, Iroise
    et al.
    Roggeman, Chantal
    Ziermans, Tim
    Peyrard-Janvid, Myriam
    Matsson, Hans
    Kere, Juha
    Klingberg, Torkel
    Influence of the COMT genotype on working memory and brain activity changes during development.2011Inngår i: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 70, nr 3, s. 222-9Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND: The Valine158Methionine (Val158Met) polymorphism of the COMT gene leads to lower enzymatic activity and higher dopamine availability in Met carriers. The Met allele is associated with better performance and reduced prefrontal cortex activation during working memory (WM) tasks in adults. Dopaminergic system changes during adolescence may lead to a reduction of basal dopamine levels, potentially affecting Met allele benefits during development.

    METHODS: We investigated the association of COMT genotype with behavioral (n = 322) and magnetic resonance imaging data (n = 81-84) collected during performance of a visuospatial WM task and potential changes in these effects during development (reflected in age × genotype interactions). Data were collected from a cross-sectional and longitudinal typically developing sample of 6- to 20-year-olds.

    RESULTS: Visuospatial WM capacity exhibited an age × genotype interaction, with a benefit of the Met allele emerging after 10 years of age. There was a parallel age × genotype interaction on WM-related activation in the right inferior frontal gyrus and intraparietal sulcus (IPS), with increases in activation with age in the Val/Val group only. Main effects of COMT genotype were also observed in the IPS, with greater gray matter volumes bilaterally and greater right IPS activation in the Val/Val group compared with the Met carriers.

    CONCLUSIONS: These results suggest that COMT genotype effects on WM brain activity and behavior are not static during development. The full developmental picture should be considered when trying to understand the impact of genetic polymorphisms on the mature cognition of healthy adult or psychiatric populations.

  • 33.
    Elgh, Eva
    et al.
    Umeå universitet, Medicinsk fakultet, Samhällsmedicin och rehabilitering, Geriatrik.
    Lindqvist Åstot, Ann
    Umeå universitet, Medicinsk fakultet, Samhällsmedicin och rehabilitering, Geriatrik.
    Fagerlund, Markku
    Umeå universitet, Medicinsk fakultet, Strålningsvetenskaper.
    Eriksson, Sture
    Umeå universitet, Medicinsk fakultet, Samhällsmedicin och rehabilitering, Geriatrik.
    Olsson, Tommy
    Umeå universitet, Medicinsk fakultet, Folkhälsa och klinisk medicin, Medicin.
    Näsman, Birgitta
    Umeå universitet, Medicinsk fakultet, Samhällsmedicin och rehabilitering.
    Cognitive dysfunction, hippocampal atrophy and glucocorticoid feedback in Alzheimer's disease.2006Inngår i: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 59, nr 2, s. 155-161Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND: The hippocampal formation is damaged early in Alzheimer's disease (AD). An association between temporal lobe volume and cognitive function has been shown in several studies. Increased limbic-hypothalamic-pituitary-adrenal (LHPA) axis function has been suggested to be related to hippocampal atrophy and cognitive impairment. Our hypothesis was that there is a clear link between hippocampal volume -- notably of the CA1 region -- memory (episodic and visuospatial) and decreased feedback sensitivity in the LHPA axis in AD. METHODS: Sixteen medication-free outpatients with mild to moderate AD were included. Hippocampal volume was measured with magnetic resonance imaging. Dexamethasone suppression tests were performed using .5 mg and .25 mg dexamethasone. Three different components in the neuropsychological battery -- Rey 15 item memory test, Alzheimer's Disease Assessment Scale (ADAS) word recall and spatial span from Wechsler Adult Intelligence Scale - Revised neuropsychological instrument (WAIS-R NI) -- were found to represent episodic and visuospatial memory. RESULTS: Low hippocampal CA1 volume and high post-dexamethasone cortisol levels in combination were significantly associated with Rey 15 item memory and spatial span test outcomes. No association was found between LHPA feedback and hippocampal volume. CONCLUSIONS: Low hippocampal volume and a disturbed negative feedback in the LHPA axis link to specific cognitive impairments in Alzheimer's disease.

  • 34.
    Endres, Dominique
    et al.
    Univ Freiburg, Dept Psychiat & Psychotherapy, Freiburg, Germany..
    Von Zedtwitz, Katharina
    Univ Freiburg, Dept Psychiat & Psychotherapy, Freiburg, Germany..
    Matteit, Isabelle
    Univ Freiburg, Dept Psychiat & Psychotherapy, Freiburg, Germany..
    Bünger, Isabel
    Univ Med Berlin, Dept Neurol & Expt Neurol, Berlin, Germany.;German Ctr Neurodegenerat Dis Berlin, Berlin, Germany..
    Foverskov-Rasmussen, Helle
    Univ Med Berlin, Dept Neurol & Expt Neurol, Berlin, Germany.;German Ctr Neurodegenerat Dis Berlin, Berlin, Germany..
    Runge, Kimon
    Univ Freiburg, Dept Psychiat & Psychotherapy, Freiburg, Germany..
    Feige, Bernd
    Univ Freiburg, Dept Psychiat & Psychotherapy, Freiburg, Germany..
    Schlump, Andrea
    Univ Freiburg, Dept Psychiat & Psychotherapy, Freiburg, Germany..
    Maier, Simon
    Univ Freiburg, Dept Psychiat & Psychotherapy, Freiburg, Germany..
    Nickel, Kathrin
    Univ Freiburg, Dept Psychiat & Psychotherapy, Freiburg, Germany..
    Berger, Benjamin
    Univ Freiburg, Clin Neurol & Neurophysiol, Med Ctr, Freiburg, Germany..
    Schiele, Miriam A.
    Univ Freiburg, Dept Psychiat & Psychotherapy, Freiburg, Germany..
    Cunningham, Janet
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Psykiatri.
    Domschke, Katharina
    Univ Freiburg, Dept Psychiat & Psychotherapy, Freiburg, Germany.;Univ Freiburg, Ctr Basics Neuromodulat, Fac Med, Freiburg, Germany..
    Prüss, Harald
    Univ Med Berlin, Dept Neurol & Expt Neurol, Berlin, Germany.;German Ctr Neurodegenerat Dis Berlin, Berlin, Germany..
    Van Elst, Ludger Tebartz
    Univ Freiburg, Dept Psychiat & Psychotherapy, Freiburg, Germany..
    Spectrum of Novel Anti-Central Nervous System Autoantibodies in the Cerebrospinal Fluid of 119 Patients With Schizophreniform and Affective Disorders2022Inngår i: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 92, nr 4, s. 261-274Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND: Autoimmune psychosis may be caused by well-characterized anti-neuronal autoantibodies, such as those against the NMDA receptor. However, the presence of additional anti-central nervous system (CNS) autoantibodies in these patients has not been systematically assessed.

    METHODS: Serum and cerebrospinal fluid (CSF) from patients with schizophreniform and affective syndromes were analyzed for immunoglobulin G anti-CNS autoantibodies using tissue-based assays with indirect immunofluorescence on unfixed murine brain tissue as part of an extended routine clinical practice. After an initial assessment of patients with red flags for autoimmune psychosis (n = 30), tissue-based testing was extended to a routine procedure (n = 89).

    RESULTS: Based on the findings from all 119 patients, anti-CNS immunoglobulin G autoantibodies against brain tissue were detected in 18% (n = 22) of patients (serum 9%, CSF 18%) following five principal patterns: 1) against vascular structures, most likely endothelial cells (serum 3%, CSF 8%); 2) against granule cells in the cerebellum and/or hippocampus (serum 4%, CSF 6%); 3) against myelinated fibers (serum 2%, CSF 2%); 4) against cerebellar Purkinje cells (serum 0%, CSF 2%); and 5) against astrocytes (serum 1%, CSF 1%). The patients with novel anti-CNS autoantibodies showed increased albumin quotients (p =.026) and white matter changes (p =.020) more frequently than those who tested negative for autoantibodies.

    CONCLUSIONS: The study demonstrates five novel autoantibody-binding patterns on brain tissue of patients with schizophreniform and affective syndromes. CSF yielded positive findings more frequently than serum analysis. The frequency and spectrum of autoantibodies in these patient groups may be broader than previously thought.

  • 35.
    Engman, Jonas
    et al.
    Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Faria, Vanda
    Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Appel, Lieuwe
    Åhs, Fredrik
    Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Linnman, Clas
    Pissiota, Anna
    Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Frans, Örjan
    Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Bani, Massimo
    Bettica, Paolo
    Pich, Emilio Merlo
    Jacobsson, Eva
    Wahlstedt, Kurt
    Fredrikson, Mats
    Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Furmark, Tomas
    Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Neural Correlates of Anxiety States in Patients with Social Anxiety Disorder2011Inngår i: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 69, s. 70S-70SArtikkel i tidsskrift (Annet vitenskapelig)
    Abstract [en]

    Background: In social anxiety disorder (SAD), the fear of being negatively evaluated by others can restrict individual everyday life, due to the anxiety caused by social interactions. How this anxiety is processed in the brain is only partly understood. We aimed to examine the correlations between subjective anxiety states and brain activity in a large sample of SAD patients, during an anxiety-provoking task.

    Methods: Data were merged from three randomized clinical PET-trials investigating regional cerebral blood flow (rCBF) during a public speaking task pre- and post treatment (SSRI n = 35, placebo n = 37). All participants met diagnostical criteria for SAD. rCBF was assessed with [15O]-labeled water and state anxiety was measured using the Spielberger state anxiety scale (STAI-S). These measures where then correlated using a covariate of interest approach in Statistical Parametric Mapping (SPM2).

    Results: rCBF and STAI-S scores correlated positively in the left parahippocampal gyrus and amygdala, as well as in the right premotor cortex (area 6). Negative correlations were observed in the left superior frontal gyrus, thalamus, and the right parahippocampal gyrus. Negative correlations were also found bilaterally in the cerebellum.

    Conclusions: The correlations between clinical anxiety states and brain activity were noted in areas previously demonstrated to be involved in emotional regulation and motor preparedness.

  • 36.
    Engman, Jonas
    et al.
    Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Frick, Andreas
    Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Alaie, Iman
    Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Björkstrand, Johannes
    Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Ågren, Thomas
    Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Faria, Vanda
    Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Gingnell, Malin
    Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Wallenquist, Ulrika
    Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Wahlstedt, Kurt
    Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Larsson, Elna-Marie
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för radiologi, onkologi och strålningsvetenskap, Enheten för radiologi.
    Morell, Arvid
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för radiologi, onkologi och strålningsvetenskap, Enheten för radiologi.
    Fredrikson, Mats
    Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Furmark, Tomas
    Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Altered Amygdala but not Default Mode Network Functional Connectivity in Social Anxiety Disorder2013Inngår i: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 73, nr 9, s. 79S-79SArtikkel i tidsskrift (Annet vitenskapelig)
  • 37.
    Engman, Jonas
    et al.
    Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Linnman, Clas
    Van Dijk, Koene R. A.
    Milad, Mohammed R.
    Estrogen Effects on Amygdala Resting-State Functional Connectivity2015Inngår i: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 77, nr 9, artikkel-id 644Artikkel i tidsskrift (Annet vitenskapelig)
  • 38.
    Engman, Jonas
    et al.
    Department of psychology.
    Åhs, Fredrik
    Linnman, Clas
    Palmquist Michelgård, Åsa
    Department of Neuroscience, Psychiatry, University Hospital.
    Bani, M
    Appel, L
    Fredrikson, Mats
    Furmark, Tomas
    Department of Psychology.
    Age and Sex Differences in NK1 Receptor Availability Assessed with [11C]GR2051712010Inngår i: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 67, nr 9, s. 206S-206SArtikkel i tidsskrift (Annet vitenskapelig)
  • 39.
    Engström, Christer
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Åström, Monica
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Nordqvist-Karlsson, Barbro
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Adolfsson, Rolf
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Nylander, Per- Olof
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Relationship between prophylactic effect of lithium therapy and family history of affective disorders1997Inngår i: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 42, nr 6, s. 425-433Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Lithium therapy response and age of onset (AOO) were studied in 98 patients with bipolar affective disorder (BPAD) who were divided into subgroups depending on type of family history of affective disorders. The highest (33.0 years) and lowest (25.5 years) age of onset were found in nonfamilial patients and in familial patients with a first-degree relative of BPAD, respectively. Nonfamilial patients showed the best response to lithium. There were 0.9 episodes/year off lithium compared to 0.3 episodes/year on lithium (an 88% decrease). A poorer response (a 71% decrease; a reduction from 1.39 episodes per year off lithium to 0.65 on lithium) was found in familial patients with a first-degree relative of BPAD. Differences in serum lithium values between the groups could not explain the observed differences. Thus, familial patients showed a more severe manifestation of the disease with an earlier AOO and a lower prophylactic effect of lithium.

  • 40.
    Falck-Ytter, Terje
    et al.
    Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi. Uppsala universitet, Kollegiet för avancerade studier (SCAS). Center of Neurodevelopmental Disorders, Centre for Psychiatry Research, Department of Women’s and Children’s Health, Karolinska Institutet & Stockholm Health Care Services, Region, Stockholm, Stockholm, Sweden.
    Kleberg, Johan Lundin
    Rare Diseases Research Group, Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden.;Center for Psychiatry Research, Department of Clinical Neuroscience, Karolinska Institutet & Stockholm Health Care Services, Region Stockholm, Stockholm, Sweden.;Department of Psychology, Stockholm University, Stockholm, Sweden..
    Portugal, Ana Maria
    Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi. Center of Neurodevelopmental Disorders, Centre for Psychiatry Research, Department of Women’s and Children’s Health, Karolinska Institutet & Stockholm Health Care Services, Region, Stockholm, Stockholm, Sweden.
    Thorup, Emilia
    Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi. Department of Psychology, Lund University, Lund, Sweden.
    Social attention: Developmental foundations and relevance for autism spectrum disorder2023Inngår i: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 94, nr 1, s. 8-17Artikkel, forskningsoversikt (Fagfellevurdert)
    Abstract [en]

    The use of the term Social Attention (SA) in the cognitive neuroscience and developmental psychopathology literature has increased exponentially in recent years, in part motivated by the aim to understand the early development of autism spectrum disorder (ASD). Unfortunately, theoretical discussions around the term have lagged behind its various uses. Here, we evaluate SA through a review of key candidate SA phenotypes emerging early in life, from newborn gaze cueing and preference for face-like configurations to later emerging skills such as joint attention. We argue that most of the considered SA phenotypes are unlikely to represent unique socio-attentional processes but have to be understood in the broader context of bottom-up and emerging top-down (domain-general) attention. Some types of SA behaviors (e.g., initiation of joint attention) are linked to the early development of ASD, but this may reflect differences in social motivation rather than attention per se. Several SA candidates are not linked to ASD early in life, including the ones that may represent uniquely socio-attentional processes (e.g., orienting to faces, predicting others’ manual action goals). Although SA may be a useful super-ordinate category under which one can organize certain research questions, the widespread use of the term without proper definition is problematic. Characterizing gaze patterns and visual attention in infants at elevated likelihood for ASD in social contexts may facilitate early detection, but conceptual clarity regarding the underlying processes at play are needed to sharpen research questions and identify potential targets for early intervention.

    Fulltekst (pdf)
    fulltext
  • 41. Falck-Ytter, Terje
    et al.
    Kleberg, Johan Lundin
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Psykologiska institutionen, Personlighets-, social- och utvecklingspsykologi. Karolinska Institutet, Stockholm, Sweden.
    Portugal, Ana Maria
    Thorup, Emilia
    Social attention: Developmental foundations and relevance for autism spectrum disorder2023Inngår i: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 94, nr 1, s. 8-17Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    The use of the term Social Attention (SA) in the cognitive neuroscience and developmental psychopathology literature has increased exponentially in recent years, in part motivated by the aim to understand the early development of autism spectrum disorder (ASD). Unfortunately, theoretical discussions around the term have lagged behind its various uses. Here, we evaluate SA through a review of key candidate SA phenotypes emerging early in life, from newborn gaze cueing and preference for face-like configurations to later emerging skills such as joint attention. We argue that most of the considered SA phenotypes are unlikely to represent unique socio-attentional processes but have to be understood in the broader context of bottom-up and emerging top-down (domain-general) attention. Some types of SA behaviors (e.g., initiation of joint attention) are linked to the early development of ASD, but this may reflect differences in social motivation rather than attention per se. Several SA candidates are not linked to ASD early in life, including the ones that may represent uniquely socio-attentional processes (e.g., orienting to faces, predicting others’ manual action goals). Although SA may be a useful super-ordinate category under which one can organize certain research questions, the widespread use of the term without proper definition is problematic. Characterizing gaze patterns and visual attention in infants at elevated likelihood for ASD in social contexts may facilitate early detection, but conceptual clarity regarding the underlying processes at play are needed to sharpen research questions and identify potential targets for early intervention.

  • 42.
    Falkmer, Marita
    et al.
    Jönköping University, Högskolan för lärande och kommunikation, HLK, CHILD.
    Stuart, G
    Danielsson, H
    Brahm, S
    Lönebrink, M
    Falkmer, Torbjörn
    Jönköping University, Hälsohögskolan, HHJ, Avd. för rehabilitering.
    Visual acuity in adults with Asperger's syndrome: No evidence for "eagle-eyed" vision2011Inngår i: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 70, nr 812, s. 812-816Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: Autism spectrum conditions (ASC) are defined by criteria comprising impairments in social interaction and communication. Altered visual perception is one possible and often discussed cause of difficulties in social interaction and social communication. Recently, Ashwin et al. suggested that enhanced ability in local visual processing in ASC was due to superior visual acuity, but that study has been the subject of methodological criticism, placing the findings in doubt.

    Methods: The present study investigated visual acuity thresholds in 24 adults with Asperger’s syndrome and compared their results with 25 control subjects with the 2 Meter 2000 Series Revised ETDRS Chart.

    Results: The distribution of visual acuities within the two groups was highly similar, and none of the participants had superior visual acuity.

    Conclusions: Superior visual acuity in individuals with Asperger’s syndrome could not be established, suggesting that differences in visual perception in ASC are not explained by this factor. A continued search for explanations of superior ability in local visual processing in persons with ASC is therefore warranted.

  • 43.
    Falkmer, Marita
    et al.
    Jönköping University.
    Stuart, Geoffrey W.
    La Trobe University Melbourne, Australia.
    Danielsson, Henrik
    Linköpings universitet, Institutet för handikappvetenskap (IHV). Linköpings universitet, Institutionen för beteendevetenskap och lärande, Handikappvetenskap. Linköpings universitet, Filosofiska fakulteten.
    Bram, Staffan
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Rehabiliteringsmedicin. Linköpings universitet, Hälsouniversitetet.
    Lönebrink, Mikael
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Rehabiliteringsmedicin. Linköpings universitet, Hälsouniversitetet.
    Falkmer, Torbjörn
    Jönköping University.
    Visual Acuity in Adults with Asperger’s Syndrome: No Evidence for “Eagle-Eyed” Vision2011Inngår i: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 70, nr 9, s. 812-816Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: Autism spectrum conditions (ASC) are defined by criteria comprising impairments in social interaction and communication.Altered visual perception is one possible and often discussed cause of difficulties in social interaction and social communication. Recently,Ashwin et al. suggested that enhanced ability in local visual processing in ASC was due to superior visual acuity, but that study has been thesubject of methodological criticism, placing the findings in doubt.

    Methods: The present study investigated visual acuity thresholds in 24 adults with Asperger’s syndrome and compared their results with 25control subjects with the 2 Meter 2000 Series Revised ETDRS Chart.

    Results: The distribution of visual acuities within the two groups was highly similar, and none of the participants had superior visual acuity.

    Conclusions: Superior visual acuity in individuals with Asperger’s syndrome could not be established, suggesting that differences in visualperception in ASC are not explained by this factor.Acontinued search for explanations of superior ability in local visual processing in personswith ASC is therefore warranted.

  • 44.
    Faraone, Stephen
    et al.
    SUNY Upstate Medical University, Syracuse NY, USA.
    James, Yanli Zhang
    SUNY Upstate Medical University, Syracuse NY, USA.
    Chen, Qi
    Örebro University, Örebro, Sweden.
    Larsson, Henrik
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Predicting Comorbid Disorders in ADHD Using Machine Learning2019Inngår i: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 85, nr 10, s. S6-S6Artikkel i tidsskrift (Annet vitenskapelig)
  • 45.
    Fernández de la Cruz, Lorena
    et al.
    Department of Clinical Neuroscience, Centre for Psychiatry Research, Stockholm, Sweden.
    Rydell, Mina
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Runeson, Bo
    Department of Clinical Neuroscience, Centre for Psychiatry Research, Stockholm, Sweden; Stockholm Health Care Services, Stockholm County Council, Stockholm, Sweden.
    Brander, Gustaf
    Department of Clinical Neuroscience, Centre for Psychiatry Research, Stockholm, Sweden.
    Rück, Christian
    Department of Clinical Neuroscience, Centre for Psychiatry Research, Stockholm, Sweden.
    D'Onofrio, Brian M
    Department of Psychological and Brain Sciences, Indiana University, Bloomington IN, USA.
    Larsson, Henrik
    Örebro universitet, Institutionen för medicinska vetenskaper. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Lichtenstein, Paul
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Mataix-Cols, David
    Department of Clinical Neuroscience, Centre for Psychiatry Research, Stockholm, Sweden; Stockholm Health Care Services, Stockholm County Council, Stockholm, Sweden.
    Suicide in Tourette's and Chronic Tic Disorders2017Inngår i: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 82, nr 2, s. 111-118Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: Persons with neuropsychiatric disorders are at increased risk of suicide, but there is little data concerning Tourette's and chronic tic disorders (TD/CTD). We aimed to quantify the risk of suicidal behavior in a large nationwide cohort of patients with TD/CTD, establish the contribution of psychiatric comorbidity to this risk, and identify predictors of suicide.

    Methods: Using a validated algorithm, we identified 7736 TD/CTD cases in the Swedish National Patient Register during a 44-year period (1969-2013). Using a matched case-cohort design, patients were compared with general population control subjects (1:10 ratio). Risk of suicidal behavior was estimated using conditional logistic regressions. Predictors of suicidal behavior in the TD/CTD cohort were studied using Cox regression models.

    Results: In unadjusted models, TD/CTD patients, compared with control subjects, had an increased risk of both dying by suicide (odds ratio: 4.39; 95% confidence interval [CI]: 2.89-6.67) and attempting suicide (odds ratio: 3.86; 95% CI: 3.50-4.26). After adjusting for psychiatric comorbidities, the risk was reduced but remained substantial. Persistence of tics beyond young adulthood and a previous suicide attempt were the strongest predictors of death by suicide in TD/CTD patients (hazard ratio: 11.39; 95% CI: 3.71-35.02, and hazard ratio: 5.65; 95% CI: 2.21-14.42, respectively).

    Conclusions: TD/CTD are associated with substantial risk of suicide. Suicidal behavior should be monitored in these patients, particularly in those with persistent tics, history of suicide attempts, and psychiatric comorbidities. Preventive and intervention strategies aimed to reduce the suicidal risk in this group are warranted.

  • 46. Fetissov, Sergueï O
    et al.
    Hallman, Jarmila
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap.
    Nilsson, Ida
    Lefvert, Ann-Kari
    Oreland, Lars
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap.
    Hökfelt, Tomas
    Aggressive behavior linked to corticotropin-reactive autoantibodies2006Inngår i: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 60, nr 8, s. 799-802Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND: Altered stress response is characteristic for subjects with abnormal aggressive and antisocial behavior, but the underlying biological mechanisms are unclear. We hypothesized that autoantibodies (autoAbs) directed against several stress-related neurohormones may exist in aggressive subjects. METHODS: Using enzyme-linked immunosorbent assay, we studied whether autoAbs directed against corticotropin (ACTH), alpha-melanocyte-stimulating hormone (alpha-MSH), oxytocin, and vasopressin are present in serum of male subjects with conduct disorder and prisoners with history of violence. Healthy blood donors served as control subjects. RESULTS: Both conduct disorder and prisoners groups displayed strongly increased levels of ACTH-reactive immunoglobulin G (IgG) and immunoglobulin M (IgM) autoAbs compared with control subjects. Levels of oxytocin-reactive IgM autoAbs were slightly increased in both groups of aggressive subjects, whereas levels of vasopressin-reactive IgG and IgM autoAbs were lower only in conduct disorder. No differences in the levels of alpha-MSH-reactive autoAbs were found between aggressive and control subjects. CONCLUSIONS: High levels of ACTH-reactive autoAbs as well as altered levels of oxytocin- and vasopressin-reactive autoAbs found in aggressive subjects may interfere with the neuroendocrine mechanisms of stress and motivated behavior. Our data suggest a new biological mechanism of human aggressive behavior that involves autoAbs directed against several stress-related neurohormones.

  • 47.
    Fischer, Håkan
    et al.
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Centrum för forskning om äldre och åldrande (ARC), (tills m KI).
    Nyberg, Lars
    Karlsson, Sari
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Centrum för forskning om äldre och åldrande (ARC), (tills m KI).
    Karlsson, Per
    Brehmer, Yvonne
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Centrum för forskning om äldre och åldrande (ARC), (tills m KI).
    Rieckmann, Anna
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Centrum för forskning om äldre och åldrande (ARC), (tills m KI).
    MacDonald, Stuart W S
    Farde, Lars
    Bäckman, Lars
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Centrum för forskning om äldre och åldrande (ARC), (tills m KI).
    Simulating neurocognitive aging: effects of a dopaminergic antagonist on brain activity during working memory2010Inngår i: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 67, nr 6, s. 575-580Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND: Previous correlational studies have indirectly linked dysfunctional dopaminergic neurotransmission to age-related cognitive deficits and associated reductions in task-induced functional brain activity. METHODS: We used an experimental-pharmacological functional magnetic resonance imaging (fMRI) approach to more directly examine the role of dopamine in neurocognitive aging. Twenty younger and 20 healthy older adults were included. During fMRI scanning, a spatial working memory (SWM) task was administered under two conditions, varying in cognitive load. Positron emission tomography measurements with the D1 receptor antagonist [(11)C]SCH23390 confirmed that a given experimental dose of unlabeled solution occupied 50% of D1 receptors in younger adults. RESULTS: An age-related reduction in SWM performance was observed, and fMRI data revealed that, relative to younger adults under placebo conditions, elderly persons under-recruited load-sensitive fronto-parietal regions during SWM. Critically, in younger adults, the D1 antagonist resulted in a similar reduction in SWM performance and fMRI response. CONCLUSIONS: These results suggest that depletion of dopamine, whether ontogenetically or pharmacologically, results in decreased SWM performance as well as reduced load-dependent modulation of the blood oxygen level dependent signal in fronto-parietal regions, possibly by decreasing the signal-to-noise ratio in relevant neural networks.

  • 48.
    Fischer, Håkan
    et al.
    Karolinska Institute.
    Nyberg, Lars
    Umeå universitet, Medicinska fakulteten, Institutionen för strålningsvetenskaper, Diagnostisk radiologi. Umeå universitet, Medicinska fakulteten, Umeå centrum för funktionell hjärnavbildning (UFBI). Umeå universitet, Medicinska fakulteten, Institutionen för integrativ medicinsk biologi (IMB).
    Karlsson, Sari
    Karolinska Institute.
    Karlsson, Per
    Karolinska Hospital.
    Brehmer, Yvonne
    Karolinska Institute.
    Rieckmann, Anna
    Karolinska Institute.
    Macdonald, Stuart WS
    University of Victoria.
    Farde, Lars
    Karolinska Hospital.
    Bäckman, Lars
    Karolinska Institute.
    Simulating neurocognitive aging: effects of a dopaminergic antagonist on brain activity during working memory2010Inngår i: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 67, nr 6, s. 575-580Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND: Previous correlational studies have indirectly linked dysfunctional dopaminergic neurotransmission to age-related cognitive deficits and associated reductions in task-induced functional brain activity.

    METHODS: We used an experimental-pharmacological functional magnetic resonance imaging (fMRI) approach to more directly examine the role of dopamine in neurocognitive aging. Twenty younger and 20 healthy older adults were included. During fMRI scanning, a spatial working memory (SWM) task was administered under two conditions, varying in cognitive load. Positron emission tomography measurements with the D1 receptor antagonist [(11)C]SCH23390 confirmed that a given experimental dose of unlabeled solution occupied 50% of D1 receptors in younger adults.

    RESULTS: An age-related reduction in SWM performance was observed, and fMRI data revealed that, relative to younger adults under placebo conditions, elderly persons under-recruited load-sensitive fronto-parietal regions during SWM. Critically, in younger adults, the D1 antagonist resulted in a similar reduction in SWM performance and fMRI response.

    CONCLUSIONS: These results suggest that depletion of dopamine, whether ontogenetically or pharmacologically, results in decreased SWM performance as well as reduced load-dependent modulation of the blood oxygen level dependent signal in fronto-parietal regions, possibly by decreasing the signal-to-noise ratio in relevant neural networks.

  • 49.
    Frick, Andreas
    et al.
    Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Engman, Jonas
    Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Alaie, Iman
    Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Björkstrand, Johannes
    Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Faria, Vanda
    Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Gingnell, Malin
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kvinnors och barns hälsa, Obstetrik & gynekologi. Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Wallenquist, Ulrika
    Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Wahlstedt, Kurt
    Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Fredrikson, Mats
    Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Furmark, Tomas
    Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Regional Gray Matter Volume of the Lingual Gyrus is Related to Symptom Severity in Patients with Social Anxiety Disorder2013Inngår i: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 73, nr 9, s. 79S-80SArtikkel i tidsskrift (Annet vitenskapelig)
  • 50.
    Frick, Andreas
    et al.
    Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Engman, Jonas
    Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Alaie, Iman
    Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Björkstrand, Johannes
    Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Gingnell, Malin
    Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Larsson, Elna-Marie
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för radiologi, onkologi och strålningsvetenskap, Enheten för radiologi.
    Morell, Arvid
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för radiologi, onkologi och strålningsvetenskap, Enheten för radiologi.
    Wahlstedt, Kurt
    Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Fredrikson, Mats
    Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Furmark, Tomas
    Uppsala universitet, Humanistisk-samhällsvetenskapliga vetenskapsområdet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Predicting Outcome of Combined CBT and SSRI Treatment for Social Anxiety Disorder Using a Machine Learning Approach2014Inngår i: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 75, nr 9, s. 357S-357SArtikkel i tidsskrift (Annet vitenskapelig)
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