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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: 2019-02-11Bibliographically 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: 2019-02-18Bibliographically 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)30562581 (PubMedID)
Available from: 2019-02-06 Created: 2019-02-06 Last updated: 2019-02-07Bibliographically 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, ISSN 0036-8156, 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: 2018-10-31Bibliographically approved
Gaudio, S., Olivo, G., Zobel, B. B. & Schiöth, H. B. (2018). Altered cerebellar-insular-parietal-cingular subnetwork in adolescents in the earliest stages of anorexia nervosa: a network-based statistic analysis. Translational Psychiatry, 8, Article ID 127.
Open this publication in new window or tab >>Altered cerebellar-insular-parietal-cingular subnetwork in adolescents in the earliest stages of anorexia nervosa: a network-based statistic analysis
2018 (English)In: Translational Psychiatry, ISSN 2158-3188, E-ISSN 2158-3188, Vol. 8, article id 127Article in journal (Refereed) Published
Abstract [en]

To date, few functional magnetic resonance imaging (fMRI) studies have explored resting-state functional connectivity (RSFC) in long-lasting anorexia nervosa (AN) patients via graph analysis. The aim of the present study is to investigate, via a graph approach (i.e., the network-based statistic), RSFC in a sample of adolescents at the earliest stages of AN (i.e., AN duration less than 6 months). Resting-state fMRI data was obtained from 15 treatment-naive female adolescents with AN restrictive type (AN-r) in its earliest stages and 15 age-matched healthy female controls. A network-based statistic analysis was used to isolate networks of interconnected nodes that differ between the two groups. Group comparison showed a decreased connectivity in a sub-network of connections encompassing the left and right rostral ACC, left paracentral lobule, left cerebellum (10th sub-division), left posterior insula, left medial fronto-orbital gyrus, and right superior occipital gyrus in AN patients. Results were not associated to alterations in intranodal or global connectivity. No sub-networks with an increased connectivity were identified in AN patients. Our findings suggest that RSFC may be specifically affected at the earliest stages of AN. Considering that the altered sub-network comprises areas mainly involved in somatosensory and interoceptive information and processing and in emotional processes, it could sustain abnormal integration of somatosensory and homeostatic signals, which may explain body image disturbances in AN. Further studies with larger samples and longitudinal designs are needed to confirm our findings and better understand the role and consequences of such functional alterations in AN.

Place, publisher, year, edition, pages
NATURE PUBLISHING GROUP, 2018
National Category
Radiology, Nuclear Medicine and Medical Imaging Psychiatry
Identifiers
urn:nbn:se:uu:diva-361277 (URN)10.1038/s41398-018-0173-z (DOI)000438104500001 ()29980676 (PubMedID)
Available from: 2018-09-27 Created: 2018-09-27 Last updated: 2018-09-27Bibliographically approved
Titova, O. E., Lindberg, E., Elmstahl, S., Lind, L., Schiöth, H. B. & Benedict, C. (2018). Associations Between the Prevalence of Metabolic Syndrome and Sleep Parameters Vary by Age. Frontiers in Endocrinology, 9, Article ID 234.
Open this publication in new window or tab >>Associations Between the Prevalence of Metabolic Syndrome and Sleep Parameters Vary by Age
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2018 (English)In: Frontiers in Endocrinology, ISSN 1664-2392, E-ISSN 1664-2392, Vol. 9, article id 234Article in journal (Refereed) Published
Abstract [en]

Objective: To examine whether the relationship between the metabolic syndrome (MetS) and various sleep parameters [sleep duration, symptoms of sleep-disordered breathing (SDB), and sleep disturbances] varies by age. Methods: Waist circumference, blood pressure, triglycerides, high-density lipoprotein cholesterol, and fasting glucose were used to determine MetS status in a cohort (N = 19,691) of middle-aged (aged 45-64 years) and older (aged >= 65 years) subjects. Habitual sleep duration (short, <= 6 h/day; normal, 7-8 h/day; and long >= 9 h/day), sleep disturbances (such as problems with falling and staying asleep), and symptoms of sleep-disordered breathing (SDB, such as snoring and sleep apneas) were measured by questionnaires. Results: Among the participants, 4,941 subjects (25.1%) fulfilled the criteria for MetS. In the entire sample, both short and long sleep durations were associated with higher prevalence of MetS as compared to normal sleep duration. When stratified by age, a similar pattern was observed for middle-aged subjects (<65 years old; prevalence ratio (PR) [95% CI], 1.13 [1.06-1.22] for short sleep and 1.26 [1.06-1.50] for long sleep duration). In contrast, in older individuals (>= 65 years old), only long sleep duration was linked to a higher prevalence of MetS (1.26 [1.12-1.42]; P < 0.01 for sleep duration x age). In the entire cohort, having at least one SDB symptom >= 4 times per week was linked to an increased prevalence of MetS; however, the PR was higher in middle-aged subjects compared with older subjects (1.50 [1.38-1.63] vs. 1.36 [1.26-1.47], respectively; P < 0.001 for SDB x age). Finally, independent of subjects' age, reports of sleep disturbances (i.e., at least one symptom >= 4 times per week) were associated with a higher likelihood of having MetS (1.12 [1.06-1.18]; P > 0.05 for sleep disturbance x age). Conclusion: Our results suggest that age may modify the associations between some sleep parameters and the prevalence of MetS.

Keywords
sleep duration, sleep disturbance, sleep-disordered breathing, metabolic syndrome, age
National Category
Respiratory Medicine and Allergy
Identifiers
urn:nbn:se:uu:diva-356873 (URN)10.3389/fendo.2018.00234 (DOI)000431867800001 ()29867766 (PubMedID)
Funder
Swedish Research Council, 2015-03100The Swedish Brain FoundationNovo Nordisk, NNF14OC0009349
Available from: 2018-08-09 Created: 2018-08-09 Last updated: 2019-01-17Bibliographically approved
Olivo, G., Solstrand Dahlberg, L., Wiemerslage, L., Swenne, I., Zhukovsky, C., Salonen-Ros, H., . . . Schiöth, H. B. (2018). Atypical anorexia nervosa is not related to brain structural changes in newly diagnosed adolescent patients.. International Journal of Eating Disorders, 51(1), 39-45
Open this publication in new window or tab >>Atypical anorexia nervosa is not related to brain structural changes in newly diagnosed adolescent patients.
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2018 (English)In: International Journal of Eating Disorders, ISSN 0276-3478, E-ISSN 1098-108X, Vol. 51, no 1, p. 39-45Article in journal (Refereed) Published
Abstract [en]

OBJECTIVE: Patients with atypical anorexia nervosa (AN) have many features overlapping with AN in terms of genetic risk, age of onset, psychopathology and prognosis of outcome, although the weight loss may not be a core factor. While brain structural alterations have been reported in AN, there are currently no data regarding atypical AN patients.

METHOD: We investigated brain structure through a voxel-based morphometry analysis in 22 adolescent females newly-diagnosed with atypical AN, and 38 age- and sex-matched healthy controls (HC). ED-related psychopathology, impulsiveness and obsessive-compulsive traits were assessed with the Eating Disorder Examination Questionnaire (EDE-Q), Barratt Impulsiveness Scale (BIS-11) and Obsessive-compulsive Inventory Revised (OCI-R), respectively. Body mass index (BMI) was also calculated.

RESULTS: Patients and HC differed significantly on BMI (p < .002), EDE-Q total score (p < .000) and OCI-R total score (p < .000). No differences could be detected in grey matter (GM) regional volume between groups.

DISCUSSION: The ED-related cognitions in atypical AN patients would suggest that atypical AN and AN could be part of the same spectrum of restrictive-ED. However, contrary to previous reports in AN, our atypical AN patients did not show any GM volume reduction. The different degree of weight loss might play a role in determining such discrepancy. Alternatively, the preservation of GM volume might indeed differentiate atypical AN from AN.

Keywords
MRI, OSFED, VBM, adolescent, anorexia, eating disorders, imaging
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:uu:diva-336179 (URN)10.1002/eat.22805 (DOI)000418270800005 ()29215777 (PubMedID)
Funder
Swedish Research Council FormasSwedish Research CouncilThe Swedish Brain Foundation
Available from: 2017-12-12 Created: 2017-12-12 Last updated: 2018-02-19Bibliographically approved
Ciuculete, D.-M., Boström, A. E., Tuunainen, A.-K., Sohrabi, F., Kular, L., Jagodic, M., . . . Schiöth, H. B. (2018). Changes in methylation within the STK32B promoter are associated with an increased risk for generalized anxiety disorder in adolescents. Journal of Psychiatric Research, 102, 44-51
Open this publication in new window or tab >>Changes in methylation within the STK32B promoter are associated with an increased risk for generalized anxiety disorder in adolescents
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2018 (English)In: Journal of Psychiatric Research, ISSN 0022-3956, E-ISSN 1879-1379, Vol. 102, p. 44-51Article in journal (Refereed) Published
Abstract [en]

Generalized anxiety disorder (GAD) is highly prevalent among adolescents. An early detection of individuals at risk may prevent later psychiatric condition. Genome-wide studies investigating single nucleotide polymorphisms (SNPs) concluded that a focus on epigenetic mechanisms, which mediate the impact of environmental factors, could more efficiently help the understanding of GAD pathogenesis. We investigated the relationship between epigenetic shifts in blood and the risk to develop GAD, evaluated by the Development and Well-Being Assessment (DAWBA) score, in 221 otherwise healthy adolescents. Our analysis focused specifically on methylation sites showing high inter-individual variation but low tissue-specific variation, in order to infer a potential correlation between results obtained in blood and brain. Two statistical methods were applied, 1) a linear model with limma and 2) a likelihood test followed by Bonferroni correction. Methylation findings were validated in a cohort of 160 adults applying logistic models against the outcome variable "anxiety treatment obtained in the past" and studied in a third cohort with regards to associated expression changes measured in monocytes. One CpG site showed 1% increased methylation in adolescents at high risk of GAD (cg16333992, P-adj. = 0.028, estimate = 3.22), as confirmed in the second cohort (p = 0.031, estimate = 1.32). The identified and validated CpG site is located within the STK32B promoter region and its methylation level was positively associated with gene expression. Gene ontology analysis revealed that STK32B is involved in stress response and defense response. Our results provide evidence that shifts in DNA methylation are associated with a modulated risk profile for GAD in adolescence.

Keywords
Epigenetics, DNA methylation, Generalized anxiety disorder, STK32B
National Category
Endocrinology and Diabetes
Identifiers
urn:nbn:se:uu:diva-361546 (URN)10.1016/j.jpsychires.2018.03.008 (DOI)000438660500008 ()29604450 (PubMedID)
Available from: 2018-10-08 Created: 2018-10-08 Last updated: 2018-10-08Bibliographically approved
Mårtensson, J., Lätt, J., Åhs, F., Fredriksson, M., Söderlund, H., Schiöth, H. B., . . . Nilsson, M. (2018). Diffusion tensor imaging and tractography of the white matter in normal aging: The rate-of-change differs between segments within tracts. Magnetic Resonance Imaging, 45, 113-119, Article ID S0730-725X(17)30059-0.
Open this publication in new window or tab >>Diffusion tensor imaging and tractography of the white matter in normal aging: The rate-of-change differs between segments within tracts
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2018 (English)In: Magnetic Resonance Imaging, ISSN 0730-725X, E-ISSN 1873-5894, Vol. 45, p. 113-119, article id S0730-725X(17)30059-0Article in journal (Refereed) Published
Abstract [en]

Knowledge concerning the normal aging of cerebral white matter will improve our understanding of abnormal changes in neurodegenerative diseases. The microstructural basis of white matter maturation and aging can be investigated using diffusion tensor imaging (DTI). Generally, diffusion anisotropy increases during childhood and adolescence followed by a decline in middle age. However, this process is subject to spatial variations between tracts. The aim of this study was to investigate to what extent age-related variations also occur within tracts. DTI parameters were compared between segments of two white matter tracts, the cingulate bundle (CB) and the inferior fronto-occipital fasciculus (IFO), in 257 healthy individuals between 13 and 84years of age. Segments of the CB and the IFO were extracted and parameters for each segment were averaged across the hemispheres. The data was analysed as a function of age. Results show that age-related changes differ both between and within individual tracts. Different age trajectories were observed in all segments of the analysed tracts for all DTI parameters. In conclusion, aging does not affect white matter tracts uniformly but is regionally specific; both between and within white matter tracts.

Keywords
Tractography, Inferior fronto-occipital fasciculus, Cingulum, Aging, White matter degeneration, White matter tract
National Category
Medical and Health Sciences Radiology, Nuclear Medicine and Medical Imaging
Identifiers
urn:nbn:se:uu:diva-319599 (URN)10.1016/j.mri.2017.03.007 (DOI)000417772500015 ()28359912 (PubMedID)
Available from: 2017-04-06 Created: 2017-04-06 Last updated: 2018-02-19Bibliographically approved
Olivo, G., Latini, F., Wiemerslage, L., Larsson, E.-M. & Schiöth, H. B. (2018). Disruption of Accumbens and Thalamic White Matter Connectivity Revealed by Diffusion Tensor Tractography in Young Men with Genetic Risk for Obesity. Frontiers in Human Neuroscience, 12, Article ID 75.
Open this publication in new window or tab >>Disruption of Accumbens and Thalamic White Matter Connectivity Revealed by Diffusion Tensor Tractography in Young Men with Genetic Risk for Obesity
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2018 (English)In: Frontiers in Human Neuroscience, ISSN 1662-5161, E-ISSN 1662-5161, Vol. 12, article id 75Article in journal (Refereed) Published
Abstract [en]

Background: Neurovascular coupling is associated with white matter (WM) structural integrity, and it is regulated by specific subtypes of dopaminergic receptors. An altered activity of such receptors, highly expressed in reward-related regions, has been reported in carriers of obesity-risk alleles of the fat mass and obesity associated (FTO) gene. Among the reward-related regions, the thalamus and the nucleus accumbens are particularly vulnerable to blood pressure dysregulation due to their peculiar anatomo-vascular characteristics, and have been consistently reported to be altered in early-stage obesity. We have thus hypothesized that a disruption in thalamus and nucleus accumbens WM microstructure, possibly on neurovascular basis, could potentially be a predisposing factor underlying the enhanced risk for obesity in the risk-allele carriers.

Methods: We have tested WM integrity in 21 male participants genotyped on the FTO risk single nucleotide polymorphisms (SNP) rs9939609, through a deterministic tractography analysis. Only homozygous participants (9 AA, 12 TT) were included. 11 tracts were selected and categorized as following according to our hypothesis: “risk tracts”, “obesity-associated tracts”, and a control tract (forcpes major). We investigated whether an association existed between genotype, body mass index (BMI) and WM microstructural integrity in the “risk-tracts” (anterior thalamic radiation and accumbofrontal fasciculus) compared to other tracts. Moreover, we explored whether WM diffusivity could be related to specific personality traits in terms of punishment and reward sensitivity, as measure by the BIS/BAS questionnaire.

Results: An effect of the genotype and an interaction effect of genotype and BMI were detected on the fractional anisotropy (FA) of the “risk tracts”. Correlations between WM diffusivity parameters and measures of punishment and reward sensitivity were also detected in many WM tracts of both networks.

Conclusions: A disruption of the structural connectivity from the nucleus accumbens and the thalamus might occur early in carriers of the FTO AA risk-allele, and possibly act as a predisposing factor to the development of obesity.

Keywords
DTI, FTO, MRI, accumbens, obesity, thalamus, tractography, white matter
National Category
Neurosciences
Identifiers
urn:nbn:se:uu:diva-346993 (URN)10.3389/fnhum.2018.00075 (DOI)000425773500001 ()29520227 (PubMedID)
Funder
Swedish Research CouncilThe Swedish Brain Foundation
Available from: 2018-03-23 Created: 2018-03-23 Last updated: 2018-04-12Bibliographically approved
Organisations
Identifiers
ORCID iD: ORCID iD iconorcid.org/0000-0001-7112-0921

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