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Rångtell, F. H., Karamchedu, S., Andersson, P., Liethof, L., Bucaro, M. O., Lampola, L., . . . Benedict, C. (2019). A single night of sleep loss impairs objective but not subjective working memory performance in a sex-dependent manner. Journal of Sleep Research, 28(1), Article ID e12651.
Open this publication in new window or tab >>A single night of sleep loss impairs objective but not subjective working memory performance in a sex-dependent manner
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2019 (English)In: Journal of Sleep Research, ISSN 0962-1105, E-ISSN 1365-2869, Vol. 28, no 1, article id e12651Article in journal (Refereed) Published
Abstract [en]

Acute sleep deprivation can lead to judgement errors and thereby increases the risk of accidents, possibly due to an impaired working memory. However, whether the adverse effects of acute sleep loss on working memory are modulated by auditory distraction in women and men are not known. Additionally, it is unknown whether sleep loss alters the way in which men and women perceive their working memory performance. Thus, 24 young adults (12 women using oral contraceptives at the time of investigation) participated in two experimental conditions: nocturnal sleep (scheduled between 22:30 and 06:30 hours) versus one night of total sleep loss. Participants were administered a digital working memory test in which eight-digit sequences were learned and retrieved in the morning after each condition. Learning of digital sequences was accompanied by either silence or auditory distraction (equal distribution among trials). After sequence retrieval, each trial ended with a question regarding how certain participants were of the correctness of their response, as a self-estimate of working memory performance. We found that sleep loss impaired objective but not self-estimated working memory performance in women. In contrast, both measures remained unaffected by sleep loss in men. Auditory distraction impaired working memory performance, without modulation by sleep loss or sex. Being unaware of cognitive limitations when sleep-deprived, as seen in our study, could lead to undesirable consequences in, for example, an occupational context. Our findings suggest that sleep-deprived young women are at particular risk for overestimating their working memory performance.

Place, publisher, year, edition, pages
John Wiley & Sons, 2019
Keywords
sound distraction, women and men, nocturnal wakefulness, subjective performance, cognition
National Category
Applied Psychology
Identifiers
urn:nbn:se:uu:diva-376724 (URN)10.1111/jsr.12651 (DOI)000456255400005 ()29383809 (PubMedID)
Funder
Fredrik och Ingrid Thurings StiftelseSwedish Research Council, 2015-03100Åke Wiberg FoundationThe Swedish Brain Foundation, FO2016-0092Swedish Society of MedicineTore Nilsons Stiftelse för medicinsk forskningNovo Nordisk, NNF14OC0009349Erik, Karin och Gösta Selanders FoundationAFA Insurance, 140006Swedish Research Council
Available from: 2019-02-11 Created: 2019-02-11 Last updated: 2019-04-23Bibliographically approved
Gaudio, S., Carducci, F., Piervincenzi, C., Olivo, G. & Schiöth, H. B. (2019). Altered thalamo-cortical and occipital-parietal-temporal-frontal white matter connections in patients with anorexia and bulimia nervosa: a systematic review of diffusion tensor imaging studies. Journal of Psychiatry & Neuroscience, 44(5), 324-339
Open this publication in new window or tab >>Altered thalamo-cortical and occipital-parietal-temporal-frontal white matter connections in patients with anorexia and bulimia nervosa: a systematic review of diffusion tensor imaging studies
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2019 (English)In: Journal of Psychiatry & Neuroscience, ISSN 1180-4882, E-ISSN 1488-2434, Vol. 44, no 5, p. 324-339Article, review/survey (Refereed) Published
Abstract [en]

Background: Anorexia nervosa and bulimia nervosa are complex mental disorders, and their etiology is still not fully understood. This paper reviews the literature on diffusion tensor imaging studies in patients with anorexia nervosa and bulimia nervosa to explore the usefulness of white matter microstructural analysis in understanding the pathophysiology of eating disorders.

Methods: We followed the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines to identify diffusion tensor imaging studies that compared patients with an eating disorder to control groups. We searched relevant databases for studies published from database inception to August 2018, using combinations of select keywords. We categorized white matter tracts according to their 3 main classes: projection (i.e., thalamo-cortical), association (i.e., occipital-parietal-temporal-frontal) and commissural (e.g., corpus callosum).

Results: We included 19 papers that investigated a total of 427 participants with current or previous eating disorders and 444 controls. Overall, the studies used different diffusion tensor imaging approaches and showed widespread white matter abnormalities in patients with eating disorders. Despite differences among the studies, patients with anorexia nervosa showed mainly white matter microstructural abnormalities of thalamo-cortical tracts (i.e., corona radiata, thalamic radiations) and occipital-parietal-temporal-frontal tracts (i.e., left superior longitudinal and inferior fronto-occipital fasciculi). It was less clear whether white matter alterations persist after recovery from anorexia nervosa. Available data on bulimia nervosa were partially similar to those for anorexia nervosa.

Limitations: Study sample composition and diffusion tensor imaging analysis techniques were heterogeneous. The number of studies on bulimia nervosa was too limited to be conclusive.

Conclusion: White matter microstructure appears to be affected in anorexia nervosa, and these alterations may play a role in the pathophysiology of this eating disorder. Although we found white matter alterations in bulimia nervosa that were similar to those in anorexia nervosa, white matter changes in bulimia nervosa remain poorly investigated, and these findings were less conclusive. Further studies with longitudinal designs and multi-approach analyses are needed to better understand the role of white matter changes in eating disorders.

Place, publisher, year, edition, pages
CMA-CANADIAN MEDICAL ASSOC, 2019
National Category
Psychiatry
Identifiers
urn:nbn:se:uu:diva-394717 (URN)10.1503/jpn.180121 (DOI)000484083400005 ()30994310 (PubMedID)
Available from: 2019-10-11 Created: 2019-10-11 Last updated: 2019-10-11Bibliographically approved
Tan, X., Titova, O. E., Lindberg, E., Elmståhl, S., Lind, L., Schiöth, H. B. & Benedict, C. (2019). Association Between Self-Reported Sleep Duration and Body Composition in Middle-Aged and Older Adults. Journal of Clinical Sleep Medicine (JCSM), 15(3), 431-435
Open this publication in new window or tab >>Association Between Self-Reported Sleep Duration and Body Composition in Middle-Aged and Older Adults
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2019 (English)In: Journal of Clinical Sleep Medicine (JCSM), ISSN 1550-9389, E-ISSN 1550-9397, Vol. 15, no 3, p. 431-435Article in journal (Refereed) Published
Abstract [en]

STUDY OBJECTIVES: The current study sought to examine whether self-reported sleep duration is linked to an adverse body composition in 19,709 adults aged 45 to 75 years.

METHODS: All variables used in the current study were derived from the Swedish EpiHealth cohort study. Habitual sleep duration was measured by questionnaires. Body composition was assessed by bioimpedance. The main outcome variables were fat mass and fat-free mass (in kg). Analysis of covariance adjusting for age, sex, fat mass in the case of fat-free mass (and vice versa), leisure time physical activity, smoking, and alcohol consumption was used to investigate the association between sleep duration and body composition.

RESULTS: Short sleep (defined as ≤ 5 hours sleep per day) and long sleep (defined as 8 or more hours of sleep per day) were associated with lower fat-free mass and higher fat mass, compared with 6 to 7 hours of sleep duration (P< .05).

CONCLUSIONS: These observations could suggest that both habitual short and long sleep may contribute to two common clinical phenotypes in middle-aged and older humans, ie, body adiposity and sarcopenia. However, the observational nature of our study does not allow for causal interpretation.

Keywords
body fat, elderly, fat-free mass, middle-aged, sleep
National Category
Neurosciences
Identifiers
urn:nbn:se:uu:diva-379286 (URN)10.5664/jcsm.7668 (DOI)000461417900009 ()30853046 (PubMedID)
Funder
Swedish Research CouncilNovo Nordisk, NNF14OC0009349Swedish Research Council, 2015-03100Ernfors FoundationÅke Wiberg Foundation, M17-0088Åke Wiberg Foundation, M18-0169Fredrik och Ingrid Thurings Stiftelse, 2017-00313Fredrik och Ingrid Thurings Stiftelse, 2018-00365
Available from: 2019-03-14 Created: 2019-03-14 Last updated: 2019-04-04Bibliographically approved
Svensson, E., Apergis-Schoute, J., Burnstock, G., Nusbaum, M. P., Parker, D. & Schiöth, H. B. (2019). General Principles of Neuronal Co-transmission: Insights From Multiple Model Systems. Frontiers in Neural Circuits, 12, Article ID 117.
Open this publication in new window or tab >>General Principles of Neuronal Co-transmission: Insights From Multiple Model Systems
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2019 (English)In: Frontiers in Neural Circuits, ISSN 1662-5110, E-ISSN 1662-5110, Vol. 12, article id 117Article, review/survey (Refereed) Published
Abstract [en]

It is now accepted that neurons contain and release multiple transmitter substances. However, we still have only limited insight into the regulation and functional effects of this co-transmission. Given that there are 200 or more neurotransmitters, the chemical complexity of the nervous system is daunting. This is made more-so by the fact that their interacting effects can generate diverse non-linear and novel consequences. The relatively poor history of pharmacological approaches likely reflects the fact that manipulating a transmitter system will not necessarily mimic its roles within the normal chemical environment of the nervous system (e.g., when it acts in parallel with cotransmitters). In this article, co-transmission is discussed in a range of systems [from invertebrate and lower vertebrate models, up to the mammalian peripheral and central nervous system (CNS)] to highlight approaches used, degree of understanding, and open questions and future directions. Finally, we offer some outlines of what we consider to be the general principles of co-transmission, as well as what we think are the most pressing general aspects that need to be addressed to move forward in our understanding of co-transmission.

Place, publisher, year, edition, pages
FRONTIERS MEDIA SA, 2019
Keywords
corelease, neurotransmitter complexity, neuromodulation, neuropeptides, colocalization
National Category
Cell and Molecular Biology
Identifiers
urn:nbn:se:uu:diva-377107 (URN)10.3389/fncir.2018.00117 (DOI)000456512900001 ()30728768 (PubMedID)
Funder
Swedish Research CouncilStiftelsen Olle Engkvist Byggmästare
Available from: 2019-02-18 Created: 2019-02-18 Last updated: 2019-03-14Bibliographically approved
Olivo, G., Gour, S. & Schiöth, H. B. (2019). Low neuroticism and cognitive performance are differently associated to overweight and obesity: A cross-sectional and longitudinal UK Biobank study.. Psychoneuroendocrinology, 101, 167-174
Open this publication in new window or tab >>Low neuroticism and cognitive performance are differently associated to overweight and obesity: A cross-sectional and longitudinal UK Biobank study.
2019 (English)In: Psychoneuroendocrinology, ISSN 0306-4530, E-ISSN 1873-3360, Vol. 101, p. 167-174Article in journal (Refereed) Published
Abstract [en]

BACKGROUND: A growing body of research has linked personality traits to cognitive performance. This relationship might play a role in the predisposition toward obesity. Neuroticism and executive function seem to be particularly involved, and reduced executive function has been proposed to underlie the association of neuroticism with sedentary behaviors and fatty food consumption. Despite the link between neuroticism, cognitive functions and obesity has been largely reported, conflicting evidence exists. Moreover, information regarding other cognitive domains, and studies on overweight individuals, are still scarce.

METHODS: We examined cross-sectional associations of neuroticism and cognitive function with overweight and obesity in a sample of 170 310 individuals from the UK Biobank cohort, adjusted for sociodemographic and life-style factors. Measures on fluid intelligence (FI) (reasoning ability), trail making test (TMT) (executive function), numeric memory test and pairs matching (PM) task (short-term memory) were extracted from the database. Correlations between neuroticism and cognitive performance were explored. Moreover, we investigated whether neuroticism and executive function could predict BMI variability over time.

RESULTS: Reduced FI and short-term memory were associated with overweight and obesity, while reduced executive function was associated with obesity but not with overweight. Low neuroticism was associated with being overweight rather than lean or obese independently of gender and life-style. Furthermore, baseline neuroticism scores could predict BMI variations over 5-10 years follow-up, and high neuroticism correlated with lower cognitive performance.

CONCLUSIONS: Lower cognitive performance is associated with both overweight and obesity, except for executive function, which was only related to obesity. Neuroticism correlated with performance on most of the cognitive domains tested, supporting the link between personality and cognition. Our findings also support the role of neuroticism in leading to greater weight variability over time, rather than to overweight/obesity itself.

Keywords
Cognition, Executive function, Neuroticism, Obesity, Overweight
National Category
Nursing
Identifiers
urn:nbn:se:uu:diva-379287 (URN)10.1016/j.psyneuen.2018.11.014 (DOI)000459840000021 ()30469083 (PubMedID)
Funder
Swedish Research Council, 23482
Available from: 2019-03-14 Created: 2019-03-14 Last updated: 2019-04-12Bibliographically approved
Herrera, G., Calfa, G., Schiöth, H. B., Lasaga, M. & Scimonelli, T. (2019). Memory consolidation impairment induced by Interleukin-1 beta is associated with changes in hippocampal structural plasticity. Behavioural Brain Research, 370, Article ID 111969.
Open this publication in new window or tab >>Memory consolidation impairment induced by Interleukin-1 beta is associated with changes in hippocampal structural plasticity
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2019 (English)In: Behavioural Brain Research, ISSN 0166-4328, E-ISSN 1872-7549, Vol. 370, article id 111969Article in journal (Refereed) Published
Abstract [en]

Pro-inflammatory cytokines, particularly Interleukin-1 beta (IL-1 beta), can affect cognitive processes such as learning and memory. The aim of this study was to establish whether the effect of IL-1 beta on contextual fear memory is associated with changes in hippocampal structural plasticity. We also studied the effect of alpha-melanocyte-stimulating hormone (alpha-MSH), a potent anti-inflammatory and neuro-protective peptide. Different groups of animals were implanted bilaterally in dorsal hippocampus (DH). After recovery they were conditioned for contextual fear memory and received the different treatments (vehicle, IL-1 beta, alpha-MSH or IL-1 beta + alpha-MSH). Memory was assessed 24 hs after conditioning and immediately after rats were perfused for dendritic spine analysis. Our results show that local hippocampal administration of IL-1 beta just after memory encoding induced impairment in contextual memory and a reduction in the total density of CA1 hippocampal dendritic spines, particularly the mature ones. alpha-MSH administration reversed the IL-1 beta induced changes. The results suggest that neuro-inflammation induced by IL-1 beta interferes with experience-dependent structural plasticity in DH whereas alpha-MSH has a beneficial modulatory role in preventing this effect.

Place, publisher, year, edition, pages
ELSEVIER SCIENCE BV, 2019
Keywords
IL-1 beta, alpha-MSH, Dendritic spines, Dorsal hippocampus
National Category
Neurology Neurosciences
Identifiers
urn:nbn:se:uu:diva-390371 (URN)10.1016/j.bbr.2019.111969 (DOI)000474323900023 ()31128164 (PubMedID)
Funder
Swedish Research Council, 2016-01088
Available from: 2019-08-12 Created: 2019-08-12 Last updated: 2019-08-12Bibliographically approved
Syk, M., Ellström, S., Mwinyi, J., Schiöth, H. B., Ekselius, L., Ramklint, M. & Cunningham, J. L. (2019). Plasma levels of leptin and adiponectin and depressive symptoms in young adults. Psychiatry Research, 272, 1-7
Open this publication in new window or tab >>Plasma levels of leptin and adiponectin and depressive symptoms in young adults
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2019 (English)In: Psychiatry Research, ISSN 0165-1781, E-ISSN 1872-7123, Vol. 272, p. 1-7Article in journal (Refereed) Published
Abstract [en]

Circulating levels of adipokines are known to be associated with depression. This study aimed to investigate a possible association between leptin, adiponectin and dimensional measures of depressive symptoms in young adults with and without psychiatric illness. Total plasma adiponectin and leptin levels were measured in 194 young adults seeking psychiatric ambulatory care and 57 healthy controls. Depressive symptoms were assessed using the Montgomery-Åsberg Depression Self-Rating Scale (MADRS-S). Analysis was performed on men and women separately. P-leptin levels were significantly elevated in patients compared with controls and correlated with total MADRS-S scores in the women. Women with P-leptin in the highest quartile reached a significantly higher MADRS-S score than women in the lowest quartile, but this difference disappeared after adjusting for body mass index (BMI) and antidepressant use. MADRS-S score was associated with P-leptin in female patients without antidepressant use, independently of BMI. There was no association between P-leptin levels and current major depression. P-adiponectin levels were not associated with depressive symptoms or current major depression. The findings indicate that P-leptin levels are associated with depressive symptom severity in young women; however, the association is linked to other factors, which challenges its usefulness as a biomarker for depression in clinical psychiatry.

Keywords
Adipokines, Depression, Inflammation, Mood disorders
National Category
Psychiatry
Research subject
Psychiatry
Identifiers
urn:nbn:se:uu:diva-376540 (URN)10.1016/j.psychres.2018.11.075 (DOI)000460994400001 ()30562581 (PubMedID)
Funder
Erik, Karin och Gösta Selanders FoundationFredrik och Ingrid Thurings StiftelseStiftelsen Söderström - Königska sjukhemmetThe Swedish Medical Association
Available from: 2019-02-06 Created: 2019-02-06 Last updated: 2019-04-10Bibliographically approved
Olivo, G., Swenne, I., Zhukovsky, C., Tuunainen, A.-K., Saaid, A., Salonen-Ros, H., . . . Schiöth, H. B. (2019). Preserved white matter microstructure in adolescent patients with atypical anorexia nervosa. International Journal of Eating Disorders, 52(2), 166-174
Open this publication in new window or tab >>Preserved white matter microstructure in adolescent patients with atypical anorexia nervosa
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2019 (English)In: International Journal of Eating Disorders, ISSN 0276-3478, E-ISSN 1098-108X, Vol. 52, no 2, p. 166-174Article in journal (Refereed) Published
Abstract [en]

Objective: Patients with atypical anorexia nervosa (AN) are often in the normal-weight range at presentation; however, signs of starvation and medical instability are not rare. White matter (WM) microstructural correlates of atypical AN have not yet been investigated, leaving an important gap in our knowledge regarding the neural pathogenesis of this disorder.

Method: We investigated WM microstructural integrity in 25 drug-naive adolescent patients with atypical AN and 25 healthy controls, using diffusion tensor imaging (DTI) with a tract-based spatial statistics (TBSS) approach. Psychological variables related to the eating disorder and depressive symptoms were also evaluated by administering the eating disorder examination questionnaire (EDE-Q) and the Montgomery-angstrom sberg depression rating scale (MADRS-S) respectively, to all participants.

Results: Patients and controls were in the normal-weight range and did not differ from the body mass index standard deviations for their age. No between groups difference in WM microstructure could be detected.

Discussion: Our findings support the hypothesis that brain structural alterations may not be associated to early-stage atypical AN. These findings also suggest that previous observations of alterations in WM microstructure in full syndrome AN may constitute state-related consequences of severe weight loss. Whether the preservation of WM structure is a pathogenetically discriminant feature of atypical AN or only an effect of a less severe nutritional disturbance, will have to be verified by future studies on larger samples, possibly directly comparing AN and atypical AN.

Keywords
adolescent, anorexia nervosa, brain, cognitive neuroscience, diffusion tensor imaging, feeding and eating disorders, neuroimaging
National Category
Psychiatry
Identifiers
urn:nbn:se:uu:diva-378685 (URN)10.1002/eat.23012 (DOI)000458301700008 ()30676658 (PubMedID)
Funder
Swedish Research CouncilThe Swedish Brain Foundation
Available from: 2019-03-12 Created: 2019-03-12 Last updated: 2019-07-30Bibliographically approved
Chatzittofis, A., Boström, A., Öberg, K., Flanagan, J., Schiöth, H., Arver, S. & Jokinen, J. (2019). Testosterone, luteinizing hormone levels and methylation status in men with hypersexual disorders. Paper presented at 31st ECNP Congress, OCT 06-09, 2018, Barcelona, SPAIN. European Neuropsychopharmacology, 29, S135-S135
Open this publication in new window or tab >>Testosterone, luteinizing hormone levels and methylation status in men with hypersexual disorders
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2019 (English)In: European Neuropsychopharmacology, ISSN 0924-977X, E-ISSN 1873-7862, Vol. 29, p. S135-S135Article in journal, Meeting abstract (Other academic) Published
Place, publisher, year, edition, pages
Elsevier, 2019
National Category
Pharmacology and Toxicology
Identifiers
urn:nbn:se:uu:diva-378237 (URN)10.1016/j.euroneuro.2018.11.247 (DOI)000458400500192 ()
Conference
31st ECNP Congress, OCT 06-09, 2018, Barcelona, SPAIN
Available from: 2019-03-15 Created: 2019-03-15 Last updated: 2019-03-15Bibliographically approved
Cedernaes, J., Schonke, M., Westholm, J. O., Mi, J., Chibalin, A., Voisin, S., . . . Benedict, C. (2018). Acute sleep loss results in tissue-specific alterations in genome-wide DNA methylation state and metabolic fuel utilization in humans. Science Advances, 4(8), Article ID eaar8590.
Open this publication in new window or tab >>Acute sleep loss results in tissue-specific alterations in genome-wide DNA methylation state and metabolic fuel utilization in humans
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2018 (English)In: Science Advances, E-ISSN 2375-2548, Vol. 4, no 8, article id eaar8590Article in journal (Refereed) Published
Abstract [en]

Curtailed sleep promotes weight gain and loss of lean mass in humans, although the underlying molecular mechanisms are poorly understood. We investigated the genomic and physiological impact of acute sleep loss in peripheral tissues by obtaining adipose tissue and skeletal muscle after one night of sleep loss and after one full night of sleep. We find that acute sleep loss alters genome-wide DNA methylation in adipose tissue, and unbiased transcriptome-, protein-, and metabolite-level analyses also reveal highly tissue-specific changes that are partially reflected by altered metabolite levels in blood. We observe transcriptomic signatures of inflammation in both tissues following acute sleep loss, but changes involving the circadian clock are evident only in skeletal muscle, and we uncover molecular signatures suggestive of muscle breakdown that contrast with an anabolic adipose tissue signature. Our findings provide insight into how disruption of sleep and circadian rhythms may promote weight gain and sarcopenia.

Place, publisher, year, edition, pages
AMER ASSOC ADVANCEMENT SCIENCE, 2018
National Category
Physiology
Identifiers
urn:nbn:se:uu:diva-364473 (URN)10.1126/sciadv.aar8590 (DOI)000443498100025 ()30140739 (PubMedID)
Funder
Swedish Research Council, 2015-03100Knut and Alice Wallenberg FoundationSwedish Research Council, 2014-6888Swedish Research Council, 2016-01088Swedish Research Council, 2016-02195Swedish Research Council, 2015-4870Carl Tryggers foundation Erik, Karin och Gösta Selanders FoundationFredrik och Ingrid Thurings StiftelseLars Hierta Memorial FoundationMagnus Bergvall FoundationNovo NordiskTore Nilsons Stiftelse för medicinsk forskningSwedish Society of Medicine, SLS-694111The Swedish Brain FoundationÅke Wiberg FoundationScience for Life Laboratory - a national resource center for high-throughput molecular bioscience
Available from: 2018-10-31 Created: 2018-10-31 Last updated: 2019-03-15Bibliographically approved
Organisations
Identifiers
ORCID iD: ORCID iD iconorcid.org/0000-0001-7112-0921

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