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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.

“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.

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.

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.

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.

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.

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

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.

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.

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.

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.

The functional connectome represents a comprehensive network map of functional connectivity throughout the human brain. To date, the relationship between the organization of functional connectivity and cognitive performance measures is still poorly understood. In the present study we use resting-state functional magnetic resonance imaging (fMRI) data to explore the link between the functional connectome and working memory capacity in an individual differences design. Working memory capacity, which refers to the maximum amount of context information that an individual can retain in the absence of external stimulation, was assessed outside the MRI scanner and estimated based on behavioral data from a change detection task. Resting-state time series were analyzed by means of voxelwise degree and eigenvector centrality mapping, which are data-driven network analytic approaches for the characterization of functional connectivity. We found working memory capacity to be inversely correlated with both centrality in the right intraparietal sulcus. Exploratory analyses revealed that this relationship was putatively driven by an increase in negative connectivity strength of the structure. This resting-state connectivity finding fits previous task based activation studies that have shown that this area responds to manipulations of working memory load.

The rich club comprises a densely mutually connected set of hub regions in the brain, thought to serve as a processing and integration core. We assessed the impact of normal variation of the tryptophane hydroxylase 2 gene's promotor region (TPH2 rs4570625) on structural connectivity of the rich club pathways by means of a candidate gene association design. Tryptophane hydroxylase 2 (TPH2) is a rate-limiting enzyme in the biosynthesis of serotonin and is known to inhibit, in addition to its role as a trans-synaptic messenger, axonal and dendritic growth. The TPH2 T-variant has been associated with reduced mRNA expression and reduced serotonin levels, which may particularly influence the development of macroscale anatomical connectivity. Here, we show larger mean connectivity in the rich club in carriers of the T-variant, suggesting potential effects of upregulation of neural connectivity growth in this central core system. In addition, by edge-removal statistics, we show that the TPH2-associated higher levels of rich club connectivity are of importance for the functioning of the total structural network. The observed association is speculated to result from an effect of serotonin levels on brain development, potentially leading to stronger structural connectivity in heavily interconnected hubs.

An individual's susceptibility to everyday cognitive failure constitutes a risk factor for physical and mental health. Different factors such as inefficiency of executive functioning and high trait impulsivity have been shown to affect this susceptibility. Furthermore, twin studies indicate a high heritability of failure susceptibility revealing genetic variables as an important biological influence. We tested for a molecular genetic association between variants on the dopamine D2 receptor gene (DRD2), which relate to executive control and impulsivity, and susceptibility to everyday cognitive failure as assessed by the cognitive failure questionnaire (CFQ) in a sample of N=500 (n=140 male, n=360 female, mean age M=24.62, SD=7.98) healthy participants of central European descent. Moreover, we assessed whether trait impulsivity as measured by the Barratt impulsiveness scale (BIS-11) qualifies as a mediator between DRD2 variants and CFQ scores. We found a positive association between DRD2 variants and the CFQ. This effect was in part yet not completely mediated by trait impulsivity. The DRD2 C/C variant constitutes a protective factor for the susceptibility to everyday cognitive failure. Results point towards at least two biopsychological pathways that may explain the observed effect.

The attentional blink phenomenon (AB) describes a transient deficit in temporally selective visual attention regarding the processing of the second of two target stimuli in a rapid serial visual presentation (RSVP) task. The AB is a very prominent paradigm in the Cognitive Neurosciences that has been extensively studied by diverse psychophysiological techniques such as EEG or fMRI. Association studies from molecular genetics are scarce although the high heritability of higher cognitive functioning is proven. Only one seminal study reported an association between AB magnitude and the dopamine receptor D2 (DRD2) C957T polymorphism (Colzato et al., 2011). This functional polymorphism influences striatal D2 receptor binding affinity and thereby the efficacy of dopaminergic neurotransmission which is important for working memory and attentional processes. Colzato et al. (2011) reported that DRD2 C957T T/T-carriers exhibit a significant smaller AB than C-allele carriers. In the present study this influence of the DRD2 SNP on the AB could not be replicated in N=211 healthy participants. However, a significantly larger lag 1 sparing was observed for homozygous T/T-carriers. Moreover, carriers of at least one T-allele showed a significantly poorer performance in the identification of T1. In general, these results support the notion of a role of the dopaminergic system on the AB. However, as our results do not parallel previous findings the exact nature of this influence and its dependence on task parameters will have to be examined in further genetic association studies.

Dopaminergic activity is modulated by acetylcholine with relevance for cognitive functioning, as shown by pharmacological work in a rodent model. In humans, the two transmitter systems' joint effort on cognition has been described on the molecular genetic level: DRD2 rs6277, a single nucleotide polymorphism (SNP) on the dopamine D2 receptor gene and CHRNA4 rs1044396, a SNP on the nicotinic acetylcholine receptor gene interact on visuo-spatial and phonological working memory. The present study uses structural MRI and voxel based morphometry to extend this behavioral work to an intermediate phenotype on the neural level. We found significantly reduced gray matter volume in the right putamen in carriers of the DRD2 C/C and CHRNA4 T/T groups. This genotype combination has previously proven to be beneficial for working memory capacity. Results are in line with the idea that the two genes jointly influence the gating signals from subcortical structures to the prefrontal cortex.

Dopaminergic neurotransmission in the mesocortical system is crucial for higher order cognition. Common variation on the dopamine D2 receptor (DRD2) gene has been linked to individual differences in dopaminergic signaling and was also repeatedly associated to cognitive markers. The relationship between dopaminergic genetic variants and neurostructural properties of the mesocortical system, however, has received little attention so far. Recently, the direction of a dopaminergic manipulation was predicted from the integrity of fiber tracts between subcortical areas and the frontal lobes. Fiber tract integrity was therefore proposed as an indicator of baseline dopamine activity. This raises the question whether DRD2 variants that relate to dopamine turnaround are also linked to fiber tract integrity. In the present study we assessed associations between the DRD2 rs6277 polymorphism and subcortical connections from connectome maps derived from diffusion weighted imaging in n=105 healthy volunteers (43 males and 62 females). Carriers of the CC genotype who are characterized by elevated striatal dopamine turnaround showed higher integrity in terms of fractional anisotropy on fiber tracts between the basal ganglia and frontal regions compared to carriers of the CT and TT variant. Our results indicate that structural connectivity could serve as a conceptual link between genetically determined individual differences in dopaminergic activity and effects of dopamine challenges on executive functioning.

According to Jaak Panksepp's Affective Neuroscience Theory and the derived self-report measure, the Affective Neuroscience Personality Scales (ANPS), differences in the responsiveness of primary emotional systems form the basis of human personality. In order to investigate neuronal correlates of personality, the underlying neuronal circuits of the primary emotional systems were analyzed in the present fMRI-study by associating the ANPS to functional connectivity in the resting brain. N=120 healthy participants were invited for the present study. The results were reinvestigated in an independent, smaller sample of N=52 participants. A seed-based whole brain approach was conducted with seed-regions bilaterally in the basolateral and superficial amygdalae. The selection of seed-regions was based on meta-analytic data on affective processing and the Juelich histological atlas. Multiple regression analyses on the functional connectivity maps revealed associations with the SADNESS-scale in both samples. Functional resting-state connectivity between the left basolateral amygdala and a cluster in the postcentral gyrus, and between the right basolateral amygdala and clusters in the superior parietal lobe and subgyral in the parietal lobe was associated with SADNESS. No other ANPS-scale revealed replicable results. The present findings give first insights into the neuronal basis of the SADNESS-scale of the ANPS and support the idea of underlying neuronal circuits. In combination with previous research on genetic associations of the ANPS functional resting-state connectivity is discussed as a possible endophenotype of personality.

Recent studies from Asia provided first evidence for a molecular genetic link between serotonergic and dopaminergic neurotransmission and Internet addiction. The present report offers data on a new candidate gene in the investigation of Internet addiction-the gene coding for the nicotinic acetylcholine receptor subunit alpha 4 (CHRNA4). A case-control study was carried out. The participants were recruited from a large gene data bank, including people from the general population and from a university setting. A total of 132 participants with problematic Internet use and 132 age- and sex-matched controls participated in the study. Participants provided DNA samples and filled in the Internet Addiction Test Questionnaire. The T- variant (CC genotype) of the rs1044396 polymorphism on the CHRNA4 gene occurred significantly more frequently in the case group. Further analyses revealed that this effect was driven by females. Combined with the findings from other studies, the present data point in the direction that rs1044396 exerts pleiotropic effects on a vast range of behaviors, including cognition, emotion, and addiction.

Chronic stress and related disruption of hypothalamic-pituitary-adrenal axis reactivity is a known risk factor for depression. Besides its effects on glucocorticoids, stress also impacts the cholinergic system. Therefore, the interaction of two polymorphisms, one on the cholinergic CHRNA4 receptor gene and one on the glucocorticoid receptor gene (NR3C1), on depression was investigated. In a sample of 800 healthy participants, we genotyped for the BCL1 rs41423247 and the CHRNA4 rs1044396 single-nucleotide polymorphisms and assessed depressiveness by means of the Beck Depression Inventory. We identified a significant epistasis effect BCL1 by CHRNA4 showing that carriers of the CC genotype at the BCL1 locus who were also homozygous for the T allele at the CHRNA4 locus had the highest depression scores. This is the first evidence from molecular genetics to show that the hypothalamic-pituitary-adrenal axis and the cholinergic system--both involved in stress reactivity--represent a combined risk factor for depression.

The temporal lobe plays a major role in anxiety and depression disorders and is also of importance for trait anxiety in the non-pathological range. The present study investigates self-report data of personality dimensions linked to trait anxiety in the context of white matter tract integrity in the temporal lobes of the human brain in a large sample of N = 110 healthy participants. The results show that especially in men values for fractional anisotropy of several white matter tracts in the temporal lobe of the left hemisphere correlate substantially with individual differences in trait anxiety (depending on the tract investigated between .40 and .49). The present study shows that not only data from functional magnetic resonance imaging (fMRI), but also from structural diffusion tensor imaging (DTI) provide interesting insights into the biological foundation of human personality traits.

Perspective-taking has become a main focus of studies on moral judgments. Recent fMRI studies have demonstrated that individual differences in brain activation predict moral decision making. In particular, pharmacological studies highlighted the crucial role for the neuropeptide oxytocin in social behavior and emotional perception. In the present study N = 154 participants were genotyped for a functional polymorphism (rs2268498) in the promoter region of the OXTR gene. We found a significant difference between carriers and non-carriers of the C-allele in exculpating agents for accidental harms ( F (1,152) = 11.49, p = .001, η 2 = .07) indicating that carriers of the C-allele rated accidentally committed harm as significantly more blameworthy than non-carriers. This is the first study providing evidence for a genetic contribution to moral judgments.

AIMS: To investigate the effects of actual and expected alcohol intake on the detection and interpretation of the basic emotions happiness and anger in facial expressions. METHODS: n = 102 healthy participants performed a dynamic emotion recognition task before and after receiving a drink which contained either a moderate alcohol dose or no alcohol in a double-blind design. RESULTS: The actual alcohol intake had no effect on detecting and interpreting facial expressions. However, subjects who expected to drink alcohol judged facial expressions significantly more often as happy. No effects were observable for the recognition of anger in facial expressions. CONCLUSION: Our results corroborate recent studies that found that the belief of consuming alcohol does not increase anger recognition or aggressive behavior but decreases aggression and social stress. Language: en

Social loafing and social facilitation are stable behavioral effects that describe increased or decreased motivation, as well as effort and cooperation in teamwork as opposed to individual working situations. Recent twin studies demonstrate the heritability of cooperative behavior. Brain imaging studies have shown that reciprocity, cooperativeness, and social rewards activate reward processing areas with strong dopaminergic input, such as the ventral striatum. Thus, candidate genes for social behavior are hypothesized to affect dopaminergic neurotransmission. In the present study, we investigated the dopaminergic genetic contribution to social cooperation, especially to social loafing and social facilitation. N = 106 healthy, Caucasian subjects participated in the study and were genotyped for three polymorphisms relevant to the dopaminergic system (COMTval158met, DRD2 c957t, DRD2 rs#2283265). In addition to a main effect indicating an increased performance in teamwork situations, we found a significant interaction between a haplotype block covering both DRD2 single nucleotide polymorphisms (SNPs) (rs#6277 and rs#2283265), henceforth referred to as the DRD2-haplotype block, and the COMT val158met polymorphism (rs#4680) with social facilitation. Carriers of the DRD2 CT-haplotype block and at least one Val-allele showed a greater increase in performance in teamwork settings when compared with carriers of the CT-haplotype block and the Met/Met-genotype. Our results suggest that epistasis between COMTval158met and the two DRD2 SNPs contributes to individual differences in cooperativeness in teamwork settings.

Knock-out studies in mice suggest a role of the CHRNA4 gene in anxiety. In the present study we extend this finding to humans by means of a genetic association study. In a sample of N = 574 healthy White participants, the CHRNA4 rs1044396 polymorphism is related to the common variance of several conceptualizations of negative emotionality. Compared to carriers of at least one T-allele, carriers of the homozygous C/C genotype described themselves as more anxious and emotionally unstable on various psychometric personality questionnaires. The scope of the genetic effect is remarkable because other prominent genetic markers for anxiety show specificity for the diagnostic tool used. The present study is the first study that demonstrates the relevance of the CHRNA4 gene for negative emotionality in humans and sets a starting point for further investigations that could inform on the treatment of various affective psychiatric disorders.

Findings from twin studies yield heritability estimates of 0.50 for prosocial behaviours like empathy, cooperativeness and altruism. First molecular genetic studies underline the influence of polymorphisms located on genes coding for the receptors of the neuropeptides, oxytocin and vasopressin. However, the proportion of variance explained by these gene loci is rather low indicating that additional genetic variants must be involved. Pharmacological studies show that the dopaminergic system interacts with oxytocin and vasopressin. The present experimental study tests a dopaminergic candidate polymorphism for altruistic behaviour, the functional COMT Val158Met SNP. N = 101 healthy Caucasian subjects participated in the study. Altruism was assessed by the amount of money donated to a poor child in a developing country, after having earned money by participating in two straining computer experiments. Construct validity of the experimental data was given: the highest correlation between the amount of donations and personality was observed for cooperativeness (r = 0.32, P ≤ 0.001). Carriers of at least one Val allele donated about twice as much money as compared with those participants without a Val allele (P = 0.01). Cooperativeness and the Val allele of COMT additively explained 14.6% of the variance in donation behaviour. Results indicate that the Val allele representing strong catabolism of dopamine is related to altruism.

Contains fulltext : 90305.pdf (Publisher’s version ) (Closed access) Mounting evidence from animal studies show that the mesolimbic dopaminergic pathways are modulated by the brain-derived neurotrophic factor (BDNF). This study investigates in N = 768 healthy Caucasian participants the influence of two prominent functional single-nucleotide polymorphisms (SNPs) on the BDNF gene (BDNF Val66Met SNP) and the ankyrin repeat and kinase domain containing 1 (ANKK1) gene (DRD2 Taq Ia/ANKK1 SNP) on the personality traits of Novelty Seeking and Harm Avoidance, which are mediated, in part, through dopaminergic mesolimbic circuitry. Carriers of the 66Met + /A1 + variant scored lowest on Novelty Seeking and highest on Harm Avoidance, compared to all other genotype groups. These participants are characterized by a relatively low D-2 receptor density in the striatum and an impaired activity-dependent secretion of BDNF. This is one of the first genetic association studies to show a modulatory role for BDNF genetic variation on genetically mediated differences in the mesolimbic dopaminergic system in the context of human personality.

Loss aversion is the tendency to overweight losses compared with gains in decision situations. Several studies have investigated the neurobiological background of this phenomenon and it was found that activation in the mesolimbic-mesocortical dopamine system during a gambling decision correlates with loss aversion. In a behavioral experiment with N = 143 subjects, the present study investigates the influence of 2 functional single-nucleotide polymorphisms on the BDNF gene (BDNF Val66Met polymorphism) and ANKK1 gene (DRD2 Taq1a/ANKK1 polymorphism), that are known to affect the dopamine system, on loss aversion. Additionally, associations of alexithymia, a personality construct describing the disability to consciously experience emotions in the self, with loss aversion and with the mentioned polymorphisms were assessed using the TAS-20 questionnaire, to replicate associations that have been reported before. Results revealed a significant interaction effect of the 2 polymorphisms on loss aversion. Carriers of the genetic constellation 66Met+/A1+ had the lowest loss aversion scores, compared with all other allelic groups. According to the literature this allelic configuration is characterized by a relatively low D2/3 receptor binding in the striatum and an impaired activity-dependent secretion of BDNF. This is the first study showing that loss aversion is related to naturally occurring differences in dopamine function.

Loss aversion is a decision bias, reflecting a greater sensitivity to losses than to gains in a decision situation. Recent neuroscientific research has shown that mesocorticolimbic structures like ventromedial prefrontal cortex and the ventral striatum constitute a bidirectional neural system that processes gains and losses and exhibits a neural basis of loss aversion. On a functional and structural level, the amygdala and insula also seem to play an important role in the processing of loss averse behavior. By applying voxel-based morphometry to structural brain images in N=41 healthy participants, the current study provides further evidence for the relationship of brain structure and loss aversion. The results show a negative correlation of gray matter volume in bilateral posterior insula as well as left medial frontal gyrus with individual loss aversion. Hence, higher loss aversion is associated with lower gray matter volume in these brain areas. Both structures have been discussed to play important roles in the brain's salience network, where the posterior insula is involved in interoception and the detection of salience. The medial frontal gyrus might impact decision making through its dense connections with the anterior cingulate cortex. A possible explanation for the present finding is that structural differences in these regions alter the processing of losses and salience, possibly biasing decision making towards avoidance of negative outcomes.

Harm avoidance is a personality trait characterized by excessive worrying and fear of uncertainty, which has repeatedly been related to anxiety disorders. Converging lines of research in rodents and humans point towards an involvement of the nicotinic cholinergic system in the modulation of anxiety. Most notably, the rs1044396 polymorphism in the CHRNA4 gene, which codes for the α4 subunit of the nicotinic acetylcholine receptor, has been linked to negative emotionality traits including harm avoidance in a recent study. Against this background, we investigated the association between harm avoidance and the rs1044396 polymorphism using data from N=1673 healthy subjects, which were collected in the context of the German multi-centre study ׳Genetics of Nicotine Dependence and Neurobiological Phenotypes׳. Homozygous carriers of the C-allele showed significantly higher levels of harm avoidance than homozygous T-allele carriers, with heterozygous subjects exhibiting intermediate scores. The effect was neither modulated by age or gender nor by smoking status. By replicating previous findings in a large population-based sample for the first time, the present study adds to the growing evidence suggesting an involvement of nicotinic cholinergic mechanism in anxiety and negative emotionality, which may pose an effective target for medical treatment.

The proneness to minor errors and slips in everyday life as assessed by the Cognitive Failures Questionnaire (CFQ) constitutes a trait characteristic and is reflected in stable features of brain structure and function. It is unclear, however, how dynamic interactions of large-scale brain networks contribute to this disposition. To address this question, we performed a high model order independent component analysis (ICA) with subsequent dual regression on resting-state fMRI data from 71 subjects to extract temporal time courses describing the dynamics of 17 resting-state networks (RSN). Dynamic network interactions between all 17 RSN were assessed by linear correlations between networks' time courses. On this basis, we investigated the relationship between subject-level RSN interactions and the susceptibility to everyday cognitive failure. We found that CFQ scores were significantly correlated with the interplay of the cingulo-opercular network (CON) and a posterior parietal network which unifies clusters in the posterior cingulate, precuneus, intraparietal lobules and middle temporal regions. Specifically, a higher positive functional connectivity between these two RSN was indicative of higher proneness to cognitive failure. Both the CON and posterior parietal network are implicated in cognitive functions, such as tonic alertness and executive control. Results indicate that proper checks and balances between the two networks are needed to protect against cognitive failure. Furthermore, we demonstrate that the study of temporal network dynamics in the resting state is a feasible tool to investigate individual differences in cognitive ability and performance.

Research on empathy has a long tradition in clinical research, as deficits in empathy have been found in many mental disorders. Over decades, a large amount of measures for empathy have been developed, but in many cases these have not been analysed with respect to validity. Therefore, this paper aims to relate various assessment methods for empathy, schizotypy and autistic traits to gain knowledge on their convergent and discriminant validity.A total of N = 108 participants were tested with two of the most widespread empathy questionnaires (Interpersonal Reactivity Index, Empathy Quotient), two behavioural paradigms (Reading the Mind in the Eyes Test, Cambridge Face-Voice Battery) and a rotation task. Furthermore, questionnaires assessing schizotypal and autistic traits were administered.Results indicate convergent validity of the applied empathy self-report measures, although their association with measures of schizotypal and autistic traits is inconsistent. However, results of the behavioural testing barely correlate either with the self-report measures or among each other.The questionnaire measures of empathy seem valid and exchangeable, and therefore suitable for capturing self-reported empathy in clinical research. The behavioural paradigms cover distinct endophenotypes of empathy and should only be used for very specific research questions.

Functional connections between brain regions constitute the substrate of the human functional connectome, whose topography has been discussed as an endophenotype for psychiatric disorders. Genetic influences on the entire connectome, however, have been rarely investigated so far. We tested for connectome-wide influences of the val158met (rs4860) polymorphism on the catechol-O-methyltransferase (COMT) gene by applying formal network analysis and eigenvector centrality mapping on the voxel level to resting-state functional magnetic imaging data. This approach finds brain regions that are central in the network by aggregating local and global connectivity patterns, most importantly without the requirement to select regions or networks of interest. The COMT variant linked to high enzyme activity increased network centrality in distributed brain areas that are known to constitute the brain's default mode network. Further results also indicated a COMT influence on areas implicated in the somatomotor network. These findings are in line with the polymorphism's alleged role in cognitive processing and its role in psychotic disorders. The study is the first to demonstrate the influence of a functional and behaviorally relevant genetic variant on connectome-wide functional connectivity and is an important step toward establishing the functional connectome as an endophenotype for psychiatric and behavioral phenotypes.

The present study investigates the link between volumetric hemispheric ratios (VHRs) and personality measures in N=267 healthy participants using Eysenck's Personality Inventory-Revised (EPQ-R) and the BIS/BAS scales. A robust association between extraversion and VHRs was observed for gray matter in males but not females. Higher gray matter volume in the left than in the right hemisphere was associated with higher extraversion in males. The results are discussed in the context of positive emotionality and laterality of the human brain.

Acetylcholine (ACh) is a known modulator of several domains of cognition, among them attention, memory and learning. The neurotransmitter also influences the speed of information processing, particularly the detection of targets and the selection of suitable responses. We examined the effect of the rs1044396 (C/T) polymorphism of the gene encoding the nicotinic acetylcholine receptor α4-subunit (CHRNA4) on response speed and selective visual attention. To this end, we administered a Stroop task, a Negative priming task and an exogenous Posner-Cuing task to healthy participants (n = 157). We found that the CHRNA4 rs1044396 polymorphism modulated the average reaction times (RTs) across all three tasks. Dependent on the C allele dosage, the RTs linearly increased. Homozygous T allele carriers were always fastest, while homozygous C allele carriers were always slowest. We did not observe effects of this polymorphism on selective attention. In sum, we conclude that naturally occurring variations within the cholinergic system influence an important factor of information processing. This effect might possibly be produced by the neuromodulator system rather than the deterministic system of cortical ACh.

The ability to understand thoughts and feelings of another person is an important prerequisite for successful social interaction. One part of this ability is the recognition of emotions in the face of the counterpart. Knowledge on genetic contributions to emotion recognition is still scarce. In the present study, 105 healthy participants were experimentally tested for their ability to recognize complex emotions in faces. As prior studies outlined the importance of the oxytocin system for emotion recognition, the functional rs2268498 polymorphism on the OXTR-gene was investigated. Although there were no differences in reaction times between genotype groups, carriers of the T-allele exhibited more accurate recognition skills than subjects carrying the CC-genotype. There was no influence of gender or age. Results support recent findings, demonstrating the importance of the oxytocin system for affect processing and related social behavior.

It has been hypothesized that two distinctive forms of Internet addiction exist. Here, generalized Internet addiction refers to the problematic use of the Internet covering a broad range of Internet-related activities. In contrast, specific forms of Internet addiction target the problematic use of distinct online activities such as excessive online video gaming or activities in social networks.The present study investigates the relationship between generalized and specific Internet addiction in a cross-cultural study encompassing data from China, Taiwan, Sweden and Germany in n = 636 participants. In this study, we assessed - besides generalized Internet addiction - addictive behavior in the domains of online video gaming, online shopping, online social networks and online pornography.The results confirm the existence of distinct forms of specific Internet addiction. One exception, however, was established in five of the six samples under investigation: online social network addiction correlates in large amounts with generalized Internet addiction.In general, it is of importance to distinguish between generalized and specific Internet addiction.

The present study focuses on the neurostructural foundations of the human personality. In a large sample of 227 healthy human individuals (168 women and 59 men), we used MRI to examine the relationship between personality traits and both regional gray and white matter volume, while controlling for age and sex. Personality was assessed using the German version of the NEO Five-Factor Inventory that measures individual differences in the 'Big Five of Personality': extraversion, neuroticism, agreeableness, conscientiousness, and openness to experience. In contrast to most previous studies on neural correlates of the Big Five, we used improved processing strategies: white and gray matter were independently assessed by segmentation steps before data analysis. In addition, customized sex-specific diffeomorphic anatomical registration using exponentiated lie algebra templates were used. Our results did not show significant correlations between any dimension of the Big Five and regional gray matter volume. However, among others, higher conscientiousness scores correlated significantly with reductions in regional white matter volume in different brain areas, including the right insula, putamen, caudate, and left fusiformis. These correlations were driven by the female subsample. The present study suggests that many results from the literature on the neurostructural basis of personality should be reviewed carefully, considering the results when the sample size is larger, imaging methods are rigorously applied, and sex-related and age-related effects are controlled.

The emotion of anxiety represents one of the most studied topics in the neurosciences, in part due to its relevance for understanding the evolutionary development of the human brain and its role in the pathogenesis of psychopathological conditions. Structural magnetic resonance imaging (sMRI) has enabled mapping of the anxious human brain and has contributed substantially to the understanding of anxiety. Alongside the fields of clinical psychology/psychiatry, personality psychology aims to support the research endeavor of mapping the anxious brain and has found that individual differences in anxiety-related personality dimensions such as Neuroticism or Harm Avoidance (measured by self-report) are correlated with gray and white matter volumes in different areas of the human brain. This review reveals that structures including parts of the frontal cortex (e.g., the orbitofrontal cortex) and the temporal lobe (e.g., the hippocampus) are often associated with trait anxiety, and it points out the inconsistencies that exist in the personality-sMRI literature on human anxiety. Consequently, we suggest new research strategies to overcome the inconsistencies. This review outlines how results from animal research can guide scientists in developing testable hypotheses in search of the anxious brain. Moreover, genetic imaging is presented as an interesting approach to mapping the anxious brain.

Recent functional imaging studies that examined functional connectivity in the resting brain have demonstrated various intrinsic connectivity networks (ICNs). Certain patterns of over- and underactivity in various ICNs have been hypothesized to form the neural basis of psychiatric disorders. Furthermore, activity in the ICNs does not reflect ongoing mental activity but the maintenance of neural circuits in a ready state suggesting not only relationships between ICNs and disorders but also correlations between ICNs and personality. In the present study, we assess the relationship between trait anxiety, a well established endophenotype of anxiety disorders, and functional connectivities within the insular salience ICN in a sample of healthy female subjects. Based on a previous study that demonstrated the functional relevance of the insular salience ICN for state anxiety, we used the harm avoidance scale from the Temperament and Character Inventory (TCI) as a trait marker to demonstrate increased functional connectivity within the insular salience ICN. Specifically, the functional connectivity between the anterior insula and the anterior cingulate and between the anterior insula and the dorsolateral prefrontal cortex were positively correlated with individual harm avoidance scores. The results fit into previous work, provide evidence for a potential biomarker of anxiety disorders and, most importantly, demonstrate a direct neural correlate of the personality trait harm avoidance in the absence of external stimulation.

In the recent past, various intrinsic connectivity networks (ICN) have been identified in the resting brain. It has been hypothesized that the fronto‐parietal ICN is involved in attentional processes. Evidence for this claim stems from task‐related activation studies that show a joint activation of the implicated brain regions during tasks that require sustained attention. In this study, we used functional magnetic resonance imaging (fMRI) to demonstrate that functional connectivity within the fronto‐parietal network at rest directly relates to attention. We applied graph theory to functional connectivity data from multiple regions of interest and tested for associations with behavioral measures of attention as provided by the attentional network test (ANT), which we acquired in a separate session outside the MRI environment. We found robust statistical associations with centrality measures of global and local connectivity of nodes within the network with the alerting and executive control subfunctions of attention. The results provide further evidence for the functional significance of ICN and the hypothesized role of the fronto‐parietal attention network. Hum Brain Mapp 35:1700–1709, 2014. © 2013 Wiley Periodicals, Inc.