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0.AbstractMajor depression has been linked to alterations of the brain’s white matter architecture. Major depression has also a considerable genetic component. It is, however, unclear if genetic liability for depression relates directly to the suggested alterations at the brain level.We re-evaluated white matter fiber tract alterations in major depression and aimed to relate polygenic risk for depression in unaffected individuals to these alterations.We conducted a population-based retrospective cohort study with N=17183 participants (n=287 currently depressed, n=5536 formerly depressed, n= 13360 healthy) aged 44 to 82 from the UK Biobank imaging cohort, collected between 2015 and 2020.Depression status was assessed based on questionnaire data. We derived 27 major white matter tracts from diffusion MRI and indexed their integrity according to mean fractional anisotropy. Genetic liability for depression was quantified by polygenic scores based on three recent case-control GWAS.White matter integrity was globally reduced in depression. The reduction was most pronounced on thalamic and intracortical fiber tracts, where the reduction was observed irrespective of current symptom status. Non-depressed individuals showed already a reduction in relevant fiber tracts with increasing polygenic risk, particularly in thalamic radiations. Subsequent in-silico simulations and non-parametric tests confirmed that the polygenic association was stronger than expected given the low-level statistical dependencies between target and discovery samples. White matter integrity on thalamic and association tracts is reduced in depression irrespective of current disease status and relates to the underlying genetic risk factors in unaffected individuals. The observed statistical links between genes, brain, and disorder adhere to the definition of an intermediate phenotype at the brain level.

Many organizational principles of structural brain networks are established before birth and undergo considerable developmental changes afterwards. These include the topologically central hub regions and a densely connected rich club. While several studies have mapped developmental trajectories of brain connectivity and brain network organization across childhood and adolescence, comparatively little is known about subsequent development over the course of the lifespan. Here, we present a cross-sectional analysis of structural brain network development in N = 8,066 participants aged 5 to 80 years. Across all brain regions, structural connectivity strength followed an ‘inverted-U’-shaped trajectory with vertex in the early 30s. Connectivity strength of hub regions showed a similar trajectory and the identity of hub regions remained stable across all age groups. While connectivity strength declined with advancing age, the organization of hub regions into a rich club did not only remain intact but became more pronounced, presumingly through a selected sparing of relevant connections from age-related connectivity loss. The stability of rich club organization in the face of overall age-related decline is consistent with a “first come, last served” model of neurodevelopment, where the first principles to develop are the last to decline with age. Rich club organization has been shown to be highly beneficial for communicability and higher cognition. A resilient rich club might thus be protective of a functional loss in late adulthood and represent a neural reserve to sustain cognitive functioning in the aging brain.

The human thalamus relays sensory signals to the cortex and facilitates brain-wide communication. The thalamus is also more directly involved in sensorimotor and various cognitive functions but a full characterization of its functional repertoire, particularly in regard to its internal anatomical structure, is still outstanding. As a putative hub in the human connectome, the thalamus might reveal its functional profile only in conjunction with interconnected brain areas. We therefore developed a novel systems-level Bayesian reverse inference decoding that complements the traditional neuroinformatics approach towards a network account of thalamic function. The systems-level decoding considers the functional repertoire (i.e., the terms associated with a brain region) of all regions showing co-activations with a predefined seed region in a brain-wide fashion. Here, we used task-constrained meta-analytic connectivity-based parcellation (MACM-CBP) to identify thalamic subregions as seed regions and applied the systems-level decoding to these subregions in conjunction with functionally connected cortical regions. Our results confirm thalamic structure–function relationships known from animal and clinical studies and revealed further associations with language, memory, and locomotion that have not been detailed in the cognitive neuroscience literature before. The systems-level decoding further uncovered large thalamic-centered systems engaged in autobiographical memory and nociception. We propose this novel decoding approach as a useful tool to detect previously unknown structure–function relationships at the brain network level, and to build viable starting points for future studies.

“Executive functions” (EFs) is an umbrella term for higher cognitive functions such as working memory, inhibition, and cognitive flexibility. These functions refer to dissociable mechanisms that are also intricately related, justifying the view of EF as a unitary mental faculty. One of the most challenging theoretical problems in this field of research has been to explain how the wide range of cognitive processes subsumed as EFs are controlled without an all-powerful but ill-defined central executive in the brain. Efforts to localize control mechanisms in circumscribed brain regions have not led to breakthrough in understanding how the brain controls and regulates itself, and no single brain system underlying a ‘central executive’ has yet been identified. We discuss how a distributed control network view can help to refine our understanding of the neurophysiological mechanisms underlying EFs. In this view, executive control functions are realized by spatially distributed brain networks, thus precluding the need for a modular central executive. We further discuss how graph-theory driven analysis of brain networks offers a unique lens on this problem by providing a reference frame to study brain connectivity in EFs in a holistic way and how neuroscience network research endeavors to investigate clinical neuropathology of disrupted EFs.

Despite the substantial heritability estimates for psychological traits, their precise genetic foundation from a molecular perspective remains elusive. We summarize findings and advances from more than twenty years of research into the molecular genetics of personality and other psychological traits. We describe how the candidate gene approach has - despite its appealing theoretical foundations - often (but not always) failed to point towards replicable associations between genetic polymorphisms and behavioral traits. The genome wide analysis approach on the contrary has become more fruitful in recent years and pointed towards reliable genetic associations. Results from genome wide scan studies (GWAS) are currently leveraged to explore gene-behavior associations through genetic correlation and polygenic score prediction which are important steps towards a precision medicine where treatment options are tailored to a patient's individual biology. But it is also true that future work needs to take a closer look at GWAS findings to link the growing list of statistical associations to biopsychological theory. We argue that research strategies from the candidate gene approach can be used to address these issues - given that necessary precautions are taken to avoid the problem of false-positive associations.

The functional connectome is organized into several separable intrinsic connectivity networks (ICNs) that are thought to be the building blocks of the mind. However, it is currently not well understood how these networks are engaged by emotionally salient information, and how such engagement fits into emotion theories. The current study assessed how ICNs respond during the processing of angry and fearful faces in a large sample (N = 843) and examined how connectivity changes relate to the ICNs. All ICNs were modulated by emotional faces and showed functional interactions, a finding which is in line with the “theory of constructed emotions” that assumes that basic emotion do not arise from separable ICNs but from their interplay. We further identified a set of brain regions whose connectivity changes during the tasks suggest a special role as “affective hubs” in the brain. While hubs were located in all ICNs, we observed high selectivity for the amygdala within the subcortical network, a finding which also fits into “primary emotion” theory. The topology of hubs corresponded closely to a set of brain regions that has been implicated in anxiety disorders, pointing towards a clinical relevance of the present findings. The present data are the most comprehensive mapping of connectome-wide changes in functionally connectivity evoked by an affective processing task thus far and support two competing views on how emotions are represented in the brain, suggesting that the connectome paradigm might help with unifying the two ideas.

Zusammenfassung. Multiple Sklerose (MS) kann bereits in der mittleren Lebensphase (36 bis 55 Jahre) die berufliche Teilhabe entscheidend beeinflussen. Diese Studie untersuchte, inwieweit sich 86 MS-Erkrankte mit unterschiedlicher beruflicher Leistungseinstufung bezüglich ausgewählter Studienvariablen zum Zeitpunkt der Fragebogenerhebung (T1) und der stationären Entlassung (T0) unterschieden. Die Gesamtstichprobe zeigte leichtgradige kognitive Dysfunktionen und ausgeprägte Fatiguewerte. Mittels logistischer Regressionsanalysen prädizierten die Variablen Tonische Alertness (TAP), Motorische Fatigue (FSMC), Expanded Disability Status Scale (EDSS) und Cognitive Reserve Index questionnaire (CRIq; CRI-Arbeit) die Leistungsbeurteilung bei T0 zu 71 %. Den Variablen Krankheitsdauer, Motorische Fatigue, Selbstwirksamkeit (FERUS) und Neuropsychologischer Störungsindex gelang dies zu 67 % bei T1. Die Studienergebnisse zeigen, dass motorische Fatigue und (spezifische und globale) neuropsychologische Marker ein relevantes Erklärungspotenzial hinsichtlich der Erwerbseinstufung von MS-Erkrankten besitzen. Zudem scheint die Selbstwirksamkeit die Erwerbsfähigkeit positiv zu beeinflussen.

Attention network theory states that attention is not a unified construct but consists of three independent systems that are supported by separable distributed networks: an alerting network to deploy attentional resources in anticipation of upcoming events, an orienting network to direct attention to a cued location, and a control network to select relevant information at the expense of concurrently available information. Ample behavioral and neuroimaging evidence supports the dissociation of the three attention domains. The strong assumption that each attentional system is realized through a separable network, however, raises the question how these networks relate to the intrinsic network structure of the brain.Our understanding of brain networks has advanced majorly in the past years due to the increasing focus on brain connectivity. It is well established that the brain is intrinsically organized into several large-scale networks whose modular structure persists across task states. Existing proposals on how the presumed attention networks relate to intrinsic networks rely mostly on anecdotal and partly contradictory arguments. We addressed this issue by mapping different attention networks with highest spatial precision at the level of cifti-grayordinates. Resulting group maps were compared to the group-level topology of 23 intrinsic networks which we reconstructed from the same participants’ resting state fMRI data. We found that all attention domains recruited multiple and partly overlapping intrinsic networks and converged in the dorsal fronto-parietal and midcingulo-insular network. While we observed a preference of each attentional domain for its own set of intrinsic networks, implicated networks did not match well to those proposed in the literature. Our results indicate a necessary refinement of the attention network theory.

Across species, the neuropeptide oxytocin has been associated with affiliative and social approach behavior. It has been suggested to exert its effects by modulating neural circuitry underlying anxiety, affiliative motivation, and social salience. The present study aims to investigate differences in subregional amygdala resting-state connectivity in healthy adult carriers of different genotypes of the oxytocin receptor (OXTR) gene polymorphism rs2268498. Previous studies have associated this polymorphic locus with social cognitive and affiliative phenotypes. The amygdala qualifies as a reasonable target due to its broad implication in emotional and social cognitive processing as well as its key role in mediating the behavioral effects of oxytocin. Whole brain seed-based functional connectivity analyses for the basolateral, centromedial and superficial amygdala revealed stronger resting-state connectivity of all amygdala subregions to the fusiform and inferior occipital gyrus in TT-carriers compared to C-allele carriers. Additional modulations were found for the centromedial amygdala which showed stronger resting-state connectivity to inferior frontal regions and the insula in C-allele carriers and to brainstem regions in TT-carriers. Our findings not only show the importance of oxytocin functioning in amygdalar neuronal signaling but also emphasize the need to investigate the amygdalar subregions individually instead of the amygdala as a whole. In summary, the present study is the first to characterize the impact of genetic variation of the OXTR gene with known functional consequences on widespread changes in a functional brain network originating from the amygdala.

Based on Eysenck’s pioneering work, CNS arousal has long been considered an encouraging biological candidate that may explain individual differences in human personality. Yet, results from empirical studies remained inconclusive. Notably, the vast majority of published results have been derived from small samples, and EEG alpha power has usually served as exclusive indicator for CNS arousal. In this study, we selected N = 468 individuals of the LIFE-Adult cohort and investigated the associations between the Big Five personality traits and CNS arousal by using the low-resolution electromagnetic tomography-based analysis tool VIGALL. Our analyses revealed that subjects who reported higher levels of extraversion and openness to experience, respectively, exhibited lower levels of CNS arousal in the resting state. Bayesian and frequentist analysis results were especially convincing for openness to experience. Among the lower-order personality traits, we obtained strongest evidence for neuroticism facet ‘impulsivity’ and reduced CNS arousal. We regard these findings as well in line with the postulations of Eysenck and Zuckerman and consistent with the assumptions of the ‘arousal regulation model’. Our results also agree with meta-analytically derived effect sizes in the field of individual differences research, highlighting the need for large studies with at least several hundreds of subjects.

Susceptibility to everyday cognitive failure is often assessed in clinical and vocational settings to estimate the effectiveness of interventions or to predict performance and performance decline in stressful situations. Comparatively little is known about the relationship between cognitive failure susceptibility as quantified by the Cognitive Failure Questionnaire (CFQ) and personality factors. We examined the relationships between the CFQ and the seven personality dimensions as assessed by the Temperament and Character Inventory (TCI). Through regression analyses with out-of-sample prediction, we explained 14.8 to 17.4% of the variance in cognitive failure from the personality scores. We established the character trait self-directedness as the main inversely related predictor of everyday cognitive failure. High cognitive failure thus seems to reflect low levels of self-confidence, self-acceptance, and responsibility for one’s own actions which are the key aspects of self-directedness. This result provides evidence for the previously stated ‘complaint’ hypothesis that cognitive failure results from a poor self-image rather than a vulnerability to stress.

When people sense that another person tries to control their decisions, some people will act against the control, whereas others will not. This individual tendency to control‐averse behavior can have far‐reaching consequences, such as engagement in illegal activities or noncompliance with medical treatments. Although individual differences in control‐averse behavior have been well documented in behavioral studies, their neurological basis is less well understood. Here, we use a neural trait approach to examine whether individual differences in control‐averse behavior might be linked to stable brain‐based characteristics. To do so, we analyze the association between intrinsic connectivity networks as measured by resting state functional magnetic resonance imaging and control‐averse behavior in an economic exchange game. In this game, subjects make choices that are either free or controlled by another person, with real consequences to both interaction partners. We find that the individual level of control‐averse behavior can be positively predicted by intrinsic connectivity within the salience network, but not the central executive network or the default mode network. Specifically, subjects with a more prominent connectivity hub in the dorsal anterior cingulate cortex show greater levels of control‐averse behavior. This finding provides the first evidence that the heterogeneity in control‐averse behavior might originate in systematic differences of the stable functional brain organization.

The awareness of the consequences of consuming animal products for the environment and one’s own health has been growing in recent years. The aim of the present research project was to examine the relationship between individual differences in biologically rooted primary emotional systems arising from phylogenetically old brain areas and dietary habits including being a vegan/vegetarian or omnivore (Study 1). Additionally, the link between the Dark Triad personality traits and dietary habits was investigated (also Study 1). In Study 2 it was aimed to replicate the associations between the Dark Triad traits and dietary habits in a new sample. In total 1140 (Study 1) and 444 (Study 2) participants took part in the research project. The Affective Neuroscience Personality Scales (ANPS) were applied to assess individual differences in six primary emotional systems. The Short Dark Triad Scale (SD3) was administered to assess individual differences in Machiavellianism, psychopathy and narcissism. The eating style of participants was measured with the Eating Behavior Questionnaire (EBQ). Results of Study 1 demonstrated higher CARE, SADNESS and spirituality scores, and lower PLAY scores in vegans/vegetarians than in omnivores. However, after the sex of the participants was included in the model, the effect on CARE got weaker. Additionally, omnivores scored higher on Machiavellianism, however, this association disappeared when sex was added to the model. In Study 2, higher scores in Machiavellianism, narcissism and psychopathy were reported for the group of omnivores compared to vegans/vegetarians, however, those effects got weaker or disappeared after the sex of participants was added to the model. The present research project adds to the literature by investigating the ANPS model and the Dark Triad of personality in the context of eating style for the first time. The findings of these two studies might help to better understand how people following different types of diet, might differ in their personalities.

The present study aimed to investigate potential associations between mindfulness and two prominent “cognitive” personality questionnaires (attentional control scale (ACS) and the cognitive failures questionnaire (CFQ)). Moreover, all participants (N = 537, n = 384 females; mean age = 23.30; SD = 5.15) provided buccal swaps for genotyping a classic polymorphism (COMT Val158Met/rs4680) known to influence dopaminergic catabolism on the biochemical level, as well as cognitive functions on a psychological level. Our results show that mindfulness is robustly linked to the ACS (positively) and the CFQ (negatively). The Met/Met genotype of the COMT polymorphism was associated with lower mindfulness (F(1, 535) = 8.27, p = .004; allele level) and higher everyday cognitive failure (F(1, 535) = 9.23, p = .003; allele level). But no significant effects of COMT Val158Met genotype could be observed for attentional control. The present findings provide evidence that the genetic COMT make up of a person could in parts explain self-reported skills in mindfulness and everyday cognitive failure. Based on the direction of the results, possible underlying factors are discussed. As such, COMT effects on an affective facet, which underlies mindfulness and everyday cognitive failures but not attentional control, may drive the effects. As still only a small part of the variance in the constructs is explained by the COMT polymorphism, potentially more genetic polymorphisms should additionally be taken into account in future studies to explain more variance. Genes involved in the dopaminergic neurotransmission seem to be an optimal starting point.

Cloninger's biosocial personality theory postulates a biological basis for the basic temperaments. With respect to reward dependence (RD) characterized by a tendency to sustain rewarding behaviors and to prefer behaviors previously associated with reward, he hypothesized low noradrenaline (NA) levels. Previous endocrine and genetic association studies have supported this hypothesis. The aim of the present study was to test for an association between the functional single nucleotide polymorphism rs1611115 (C-970T) on the dopamine-β-hydroxylase (DBH) gene and RD. DBH is an enzyme crucial for the synthesis of NA by catalyzing the oxidative hydroxylation of dopamine to NA. In two independent samples (N = 1144 and N = 826) of healthy participants we found significant genotype effects (p ≤ 0.0001 and p ≤ 0.05). Carriers of the C allele had significant higher RD scores than carriers homozygous for the T allele. Although the general RD–NA hypothesis was corroborated, the directionality of the observed effect was antithetical. Based on previous functionality studies reporting low enzymatic activity related to the TT genotype, present results indicate high NA levels in subjects scoring high on RD (in contrast to Cloninger's thesis). Future studies have to analyze how DBH activity and NA levels are dependent on the availability of dopamine.

Heightened sensitivity to losses, known as loss aversion, is a putative avoidance behaviour, which commonly influences decision-making, particularly in economic scenarios where participants have a 50/50 chance of winning or losing money. Evidence from neuropsychology, EEG and TMS research suggests individual differences in loss aversion may be explained by neural differences in the lateralisation of the right hemisphere. 40 healthy participants underwent an EEG recording during resting state and subsequently performed a behavioural loss aversion task, in which they had an equal chance of winning or losing money. EEG asymmetry in the alpha band at central and posterior sites was associated with individual differences in behavioural loss aversion. This asymmetry was driven by a combination of increased activation in the right hemisphere and decreased activation in the left hemisphere and the site of this asymmetry differed for females and males. These findings are discussed in relation to behavioural avoidance.

Internet gaming disorder represents a growing health issue. Core symptoms include unsuccessful attempts to control the addictive patterns of behavior and continued use despite negative consequences indicating a loss of regulatory control. Previous studies revealed brain structural deficits in prefrontal regions subserving regulatory control in individuals with excessive Internet use. However, because of the cross-sectional nature of these studies, it remains unknown whether the observed brain structural deficits preceded the onset of excessive Internet use. Against this background, the present study combined a cross-sectional and longitudinal design to determine the consequences of excessive online video gaming. Forty-one subjects with a history of excessive Internet gaming and 78 gaming-naive subjects were enrolled in the present study. To determine effects of Internet gaming on brain structure, gaming-naive subjects were randomly assigned to 6 weeks of daily Internet gaming (training group) or a non-gaming condition (training control group). At study inclusion, excessive Internet gamers demonstrated lower right orbitofrontal gray matter volume compared with Internet gaming-naive subjects. Within the Internet gamers, a lower gray matter volume in this region was associated with higher online video gaming addiction severity. Longitudinal analysis revealed initial evidence that left orbitofrontal gray matter volume decreased during the training period in the training group as well as in the group of excessive gamers. Together, the present findings suggest an important role of the orbitofrontal cortex in the development of Internet addiction with a direct association between excessive engagement in online gaming and structural deficits in this brain region.

Oxytocin is an important messenger in the brain that has been linked to a variety of social functions in pharmacological studies. Besides, functional genetic variations on the oxytocin receptor gene have been repeatedly associated with social processing and functioning. Despite this knowledge, there are very few studies investigating the mechanisms that may explain the link between oxytocin and social functions. In the endeavor to fill this gap in the literature, the current study searches for associations between the prominent rs2268498 polymorphism on the oxytocin receptor gene and participants’ ability to perceive and store implicit social information, which is a fundamental function in social information processing. N = 121 healthy participants were experimentally tested with an implicit learning paradigm, answered questionnaires assessing empathy and autistic traits, and were genotyped for the rs2268498 polymorphism. T-allele carriers (TT and TC genotypes) exhibited significantly better implicit learning performance than carriers of the CC-genotype, and learning performance was positively associated with self-reported empathy and negatively with self-reported autistic traits. Results indicate that differences in implicit perception and storing of environmental details while watching social interactions could be an important mechanism to explain the association between differences in endogenous oxytocin activity and social functioning.

The hypothalamic neuropeptide oxytocin (OT) has received increasing attention for its role in modulating social-emotional processes across species. Previous studies on using intranasal-OT in humans point to a crucial engagement of the amygdala in the observed neuromodulatory effects of OT under task and rest conditions. However, the amygdala is not a single homogenous structure, but rather a set of structurally and functionally heterogeneous nuclei that show distinct patterns of connectivity with limbic and frontal emotion-processing regions. To determine potential differential effects of OT on functional connectivity of the amygdala subregions, 79 male participants underwent resting-state fMRI following randomized intranasal-OT or placebo administration. In line with previous studies OT increased the connectivity of the total amygdala with dorso-medial prefrontal regions engaged in emotion regulation. In addition, OT enhanced coupling of the total amygdala with cerebellar regions. Importantly, OT differentially altered the connectivity of amygdala subregions with distinct up-stream cortical nodes, particularly prefrontal/parietal, and cerebellar down-stream regions. OT-induced increased connectivity with cerebellar regions were largely driven by effects on the centromedial and basolateral subregions, whereas increased connectivity with prefrontal regions were largely mediated by right superficial and basolateral subregions. OT decreased connectivity of the centromedial subregions with core hubs of the emotional face processing network in temporal, occipital and parietal regions. Preliminary findings suggest that effects on the superficial amygdala-prefrontal pathway were inversely associated with levels of subclinical depression, possibly indicating that OT modulation may be blunted in the context of increased pathological load. Together, the present findings suggest a subregional-specific modulatory role of OT on amygdala-centered emotion processing networks in humans.

Idiopathic stuttering is a fluency disorder characterized by impairments during speech production. Deficits in the motor control circuits of the basal ganglia have been implicated in idiopathic stuttering but it is unclear how these impairments relate to the disorder. Previous work has indicated a possible deficiency in motor inhibition in children who stutter. To extend these findings to adults, we designed two experiments to probe executive motor control in people who stutter using manual reaction time tasks that do not rely on speech production. We used two versions of the stop-signal reaction time task, a measure for inhibitory motor control that has been shown to rely on the basal ganglia circuits. We show increased stop-signal reaction times in two independent samples of adults who stutter compared to age- and sex-matched control groups. Additional measures involved simple reaction time measurements and a task-switching task where no group difference was detected. Results indicate a deficiency in inhibitory motor control in people who stutter in a task that does not rely on overt speech production and cannot be explained by general deficits in executive control or speeded motor execution. This finding establishes the stop-signal reaction time as a possible target for future experimental and neuroimaging studies on fluency disorders and is a further step towards unraveling the contribution of motor control deficits to idiopathic stuttering.

Objective Fatigue and cognitive deficits are frequent symptoms of multiple sclerosis (MS). However, the exact nature of their co-occurrence is not fully understood. We sought to determine the impact of cognitive and physical fatigue on subjective cognitive deficits in MS patients and healthy controls. Methods Self-reports of fatigue (FSMC), depression (CES-D), cognitive deficits (CFQ), and personality traits (NEO-FFI, ANPS) among 30 MS inpatients and 30 healthy controls were analyzed using hierarchical regression models. The frequency of cognitive mistakes was used as the dependent variable and the extent of cognitive and physical fatigue as the independent variable. Results Cognitive fatigue was the only unique and significant predictor of cognitive mistakes in both groups, explaining 13.3% of additional variance in the MS group after correcting for age, mood, and physical fatigue. Physical fatigue had no significant impact on cognitive mistakes. While age had an impact on cognitive mistakes and depression in healthy controls, this association was not significant in MS patients. Depression was significantly correlated with cognitive mistakes and cognitive fatigue in MS patients. Conclusions The interplay of cognitive fatigue and subjective cognitive impairment can be generalized, with the exception of the variables of age and depression, which were shown to have differing impacts on cognitive mistakes in MS patients and healthy controls, respectively. Cognitive fatigue was linked to cognitive mistakes even after correcting for overlapping items in MS patients only. Future research should further investigate the link between cognitive fatigue and attention lapses in daily life by using various objective assessments.

We organized 10Kin1day, a pop-up scientific event with the goal to bring together neuroimaging groups from around the world to jointly analyze 10,000+ existing MRI connectivity datasets during a 3-day workshop. In this report, we describe the motivation and principles of 10Kin1day, together with a public release of 8,000+ MRI connectome maps of the human brain.

A prominent theory of developmental stuttering highlights (dys-)function of the basal ganglia (and in particular the ventral striatum) as a main neural mechanism behind this speech disorder. Although the theory is intriguing, studies on gray matter volume differences in the basal ganglia between people who stutter and control persons have reported heterogeneous findings, either showing more or less gray matter volume of the aforementioned brain structure across the brain's hemispheres. Moreover, some studies did not observe any differences at all.From today's perspective several of the earlier studies are rather underpowered and also used less powerful statistical approaches to investigate differences in brain structure between people who stutter and controls. Therefore, the present study contrasted a comparably larger sample of n = 36 people who stutter with n = 34 control persons and applied the state of the art DARTEL algorithm (Diffeomorphic Anatomical Registration Through Exponentiated Lie algebra) to analyze the available brain data. In the present data set stuttering was associated with higher gray matter volume of the right caudate and putamen region of the basal ganglia in patients. Our observation strongly supports a recent finding reporting a larger nucleus accumbens in the right hemisphere in people who stutter when compared to control persons. The present findings are discussed in the context of both compensatory effects of the brain and putative therapeutic effects due to treatment of stuttering. Keywords: Idiopathic stuttering, Developmental stuttering, Basal ganglia, Putamen, Caudate, Voxel based morphometry, DARTEL, Speech disorder

The brain is an intricate network, not only structurally but also functionally. On the functional level, connectivity in the brain is organized in separable yet interacting networks that support information processing by maintaining a ready state, even in the absence of external stimulation. It has been hypothesized that an insular-opercular network underlies the processing of emotionally salient information and that individual differences in functional connectivity within this network correspond to individual differences in trait anxiety. Here, we tested this relationship by applying graph analysis to multiple regions of interests delineating the insular-opercular network to estimate the characteristic path length that quantifies the overall information exchange efficiency within a given network. We found that people scoring high on the anxiety-related temperament-dimension harm avoidance had decreased insular-opercular network efficiency in the resting state, as indicated by a higher characteristic path length. Furthermore, people scoring high on harm avoidance showed generally reduced functional connectivity between brain regions; the relationship between harm avoidance and insular-opercular network efficiency remained significant when controlling for mean connectivity within this network. No such results were found for other resting-state networks. The results provide insights into how personality is organized in the human brain and point toward clinically relevant endophenotypes for affective and mood disorders.

Susceptibility to everyday cognitive failure is often assessed in clinical and vocational settings to estimate the effectiveness of interventions or to predict performance and performance decline in stressful situations. Comparatively little is known about the relationship between cognitive failure susceptibility as quantified by the Cognitive Failure Questionnaire (CFQ) and personality factors. We examined the relationships between the CFQ and the seven personality dimensions as assessed by the Temperament and Character Inventory (TCI). Through regression analyses with out-of-sample prediction in two samples, we explained around 18% of the variance in cognitive failure from personality scores. We established the character trait self-directedness as the main inversely related predictor of everyday cognitive failure. High cognitive failure thus seems to reflect low levels of self-confidence, self-acceptance, and responsibility for one's own actions which are the key aspects of self-directedness. This result provides evidence for the previously stated ‘complaint’ hypothesis that cognitive failure results from a poor self-image rather than a vulnerability to stress.

A prevailing topic in personality neuroscience is the question how personality traits are reflected in the brain. Functional and structural networks have been examined by functional and structural magnetic resonance imaging, however, the structural correlates of functionally defined networks have not been investigated in a personality context. By using the Temperament and Character Inventory (TCI) and Diffusion Tensor Imaging (DTI), the present study assesses in a sample of 116 healthy participants how personality traits proposed in the framework of the biopsychosocial theory of personality relate to white matter pathways delineated by functional network imaging. We show that the character trait self-directedness relates to the overall microstructural integrity of white matter tracts constituting the salience network as indicated by DTI-derived measures. Self-directedness has been proposed as the executive control component of personality and describes the tendency to stay focused on the attainment of long-term goals. The present finding corroborates the view of the salience network as an executive control network that serves maintenance of rules and task-sets to guide ongoing behavior.

Personality and individual differences originate from the brain. Despite major advances in the affective and cognitive neurosciences, however, it is still not well understood how personality and single personality traits are represented within the brain. Most research on brain-personality correlates has focused either on morphological aspects of the brain such as increases or decreases in local gray matter volume, or has investigated how personality traits can account for individual differences in activation differences in various tasks. Here, we propose that personality neuroscience can be advanced by adding a network perspective on brain structure and function, an endeavor that we label personality network neuroscience.With the rise of resting-state functional magnetic resonance imaging (MRI), the establishment of connectomics as a theoretical framework for structural and functional connectivity modeling, and recent advancements in the application of mathematical graph theory to brain connectivity data, several new tools and techniques are readily available to be applied in personality neuroscience. The present contribution introduces these concepts, reviews recent progress in their application to the study of individual differences, and explores their potential to advance our understanding of the neural implementation of personality.Trait theorists have long argued that personality traits are biophysical entities that are not mere abstractions of and metaphors for human behavior. Traits are thought to actually exist in the brain, presumably in the form of conceptual nervous systems. A conceptual nervous system refers to the attempt to describe parts of the central nervous system in functional terms with relevance to psychology and behavior. We contend that personality network neuroscience can characterize these conceptual nervous systems on a functional and anatomical level and has the potential do link dispositional neural correlates to actual behavior.

Interactions between oxytocin and the basal ganglia are central in current overarching conceptualizations of its broad modulatory effects on behavior. Whereas evidence from animal models emphasizes the critical role of the ventral striatum in the behavioral effects of oxytocin, region-specific contributions of the basal ganglia have not been systematically explored in humans. The present study combined the randomized placebo-controlled administration of oxytocin versus placebo in healthy men (n = 144) with fMRI-based resting-state functional connectivity to determine the modulatory role of oxytocin on the major basal ganglia pathways. Oxytocin specifically increased connectivity between ventral striatal and pallidal nodes with upstream frontal regions, whereas it decreased the strengths of downstream pathways between the dorsal striatum and posterior cerebellum. These pathways have previously been implicated in salience, reward and behavioral flexibility, thus shaping goal-directed behavior. Given the importance of aberrant striatal intrinsic organization in autism, addiction and schizophrenia the present findings may suggest new mechanistic perspectives for the therapeutic potential of oxytocin in these disorders.

Background Vicarious embarrassment (VE) is an emotion triggered by the observation of others' pratfalls or social norm violations. Several explanatory approaches have been suggested to explain the source of this phenomenon, including perspective taking abilities or ingroup identification. Knowledge about its biological bases, however, is scarce. To gain a better understanding, the present study investigated neural activation patterns in response to video clips from reality TV shows. Reality TV is well known for presenting social norm violations, flaws and pratfalls of its protagonists in real life situations thereby qualifying as an ecological valid trigger for VE. Methods N = 60 healthy participants viewed stand stills from previously watched video clips taken from German reality TV-shows while undergoing functional magnetic resonance imaging. The clips were preselected for high versus low VE content in a pilot study. Besides the investigation of differences in brain activation elicited by VE versus control stand stills (blocked design contrast), we performed additional exploratory functional connectivity analyses (psychophysiological interaction; PPI) to detect VE related brain networks. Results Compared to the low VE condition, participants in the high VE condition showed a higher activation in the middle temporal gyrus, the supramarginal gyrus, the right inferior frontal gyrus and the gyrus rectus. Functional connectivity analyses confirmed increased connectivity of these regions with the anterior cingulate in the VE condition. Moreover, self-ratings of VE and brain activity were correlated positively. Conclusion Reality TV formats with high VE content activate brain regions associated with Theory of Mind, but also with empathic concern and social identity. Therefore, our results support the idea that the ability to put oneself in other person's shoes is a major prerequisite for VE.

Pharmacological and genetic modulation of cholinergic nicotinic neurotransmission influence visuospatial attention in humans. Prior studies show that nicotine as well as a single nucleotide polymorphism (SNP) in the gene coding for the alpha 4 subunit of the nicotinic acetylcholine receptor (CHRNA4) modulate visuospatial attention and distractor interference. The CHRNA4 gene synergistically interacts with a polymorphism in the dopaminergic receptor type d2 (DRD2) gene and impacts brain structure and cognition. We aimed to investigate whether CHRNA4 and DRD2 genotypes alter the effects of nicotine on distractor interference. Fifty-eight young healthy non-smokers were genotyped for CHRNA4 (rs1044396) and DRD2 (rs6277). They received either 7 mg transdermal nicotine or a matched placebo in a double-blind, within-subject design 1 h prior to performing a visual search task with distractors. In isolation, DRD2 but not CHRNA4 genotype modulated the effects of nicotine on distractor interference with DRD2 CC carriers showing the strongest reduction of distractor interference after nicotine administration. A further analysis provided additional evidence that this effect was driven by those subjects, who carried at least one C allele in the CHRNA4 gene. The effects of nicotine on distractor interference are modulated synergistically by cholinergic and dopaminergic genetic variations. Hence, both genes may contribute to the often reported individual variability in cognitive and neural effects of nicotine.

Objective It remains an unresolved research objective to clarify the overlap/association between fatigue (especially its cognitive facet) and depression in People with MS (PwMS). Therefore, in this study the patterns of personality and primary emotional traits (PETs) associated with each (motoric/cognitive fatigue and depression in PwMS) were investigated and compared in order to disentangle the three constructs in PwMS. Additionally, differences in personality and PETs between PwMS and healthy controls (HC) were examined. Method Associations between motoric/cognitive fatigue, depression, personality and PETs were investigated in 52 PwMS. Personality and PETs were also assessed in a gender matched HC sample (N = 52) and results regarding these were compared between PwMS and HC. Results Low extraversion was the only significant predictor of MS related motoric fatigue (β = -.341, p = .013). High neuroticism was a predictor of both MS related cognitive fatigue (β = .426, p = .002) and depression (β = .443, p < .001). Whereas neuroticism was the only significant predictor for MS related cognitive fatigue, the cluster of (high) neuroticism, (high) SADNESS (β = .273, p = .023), and (low) extraversion (β = -.237, p = .025) predicted MS related depression. PwMS showed significantly higher scores in neuroticism and FEAR compared to HC. Conclusions MS related motoric/cognitive fatigue and depression in PwMS share variance. But the substantial amount of non-shared variance (motoric fatigue, depression: 72%; cognitive fatigue, depression: 66%) together with additional predictors for depression (SADNESS being a predictor of depression only), indicate that MS related motoric/cognitive fatigue and depression are distinguishable. Consequently, we recommend assessing especially SADNESS scores to distinguish between MS related fatigue and depression.

A recent study has implicated the nucleus accumbens of the ventral striatum in explaining why online-users spend time on the social network platform Facebook. Here, higher activity of the nucleus accumbens was associated with gaining reputation on social media. In the present study, we touched a related research field. We recorded the actual Facebook usage of N=62 participants on their smartphones over the course of five weeks and correlated summary measures of Facebook use with gray matter volume of the nucleus accumbens. It appeared, that in particular higher daily frequency of checking Facebook on the smartphone was robustly linked with smaller gray matter volumes of the nucleus accumbens. The present study gives additional support for the rewarding aspects of Facebook usage. Moreover, it shows the feasibility to include real life behavior variables in human neuroscientific research.