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Overweight (OW) and obesity (OB) have become prevalent issues in the global public health arena. Serving as a prominent risk factor for various chronic diseases, overweight/obesity not only poses serious threats to people's physical and mental health but also imposes significant medical and economic burdens on society as a whole. In recent years, there has been a growing focus on basic scientific research dedicated to seeking the neural evidence underlying overweight/obesity, aiming to elucidate its causes and effects by revealing functional alterations in brain networks. Among them, dysfunction in the reward network (RN) and executive control network (ECN) during both resting state and task conditions is considered pivotal in neuroscience research on overweight/obesity. Their aberrations contribute to explaining why persons with overweight/obesity exhibit heightened sensitivity to food rewards and eating disinhibition. This review centers on the reward and executive control network by analyzing and organizing the resting-state and task-based fMRI studies of functional brain network alterations in overweight/obesity. Building upon this foundation, the authors further summarize a reward-inhibition dual-system model, with a view to establishing a theoretical framework for future exploration in this field. [ABSTRACT FROM AUTHOR]

The human reward network consists of interconnected brain regions that process stimuli associated with satisfaction and modulate pleasure-seeking behaviors. Impairments in reward processing have been implicated in several medical and psychiatric conditions, and there is a growing interest in disentangling the underlying pathophysiological mechanisms. The brain–gut axis plays a regulatory role in several higher-order neurophysiological pathways, including reward processing. In this context, the aim of the current review was to critically appraise research findings on the contribution of the brain–gut axis to the human reward system. Enteric neuropeptides, which are implicated in the regulation of hunger and satiety, such as ghrelin, PYY3–36, and glucagon-like peptide 1 (GLP-1), have been associated with the processing of food-related, alcohol-related, and other non-food-related rewards, maintaining a delicate balance between the body's homeostatic and hedonic needs. Furthermore, intestinal microbiota and their metabolites have been linked to differences in the architecture and activation of brain reward areas in obese patients and patients with attention deficit and hyperactivity disorder. Likewise, bariatric surgery reduces hedonic eating by altering the composition of gut microbiota. Although existing findings need further corroboration, they provide valuable information on the pathophysiology of reward-processing impairments and delineate a novel framework for potential therapeutic interventions. [ABSTRACT FROM AUTHOR]

Algorithmic trading is playing an increasingly important role in the financial market, achieving more efficient trading strategies by replacing human decision-making. Among numerous trading algorithms, deep reinforcement learning is gradually replacing traditional high-frequency trading strategies and has become a mainstream research direction in the field of algorithmic trading. This paper introduces a novel approach that leverages reinforcement learning with human feedback (RLHF) within the double DQN algorithm. Traditional reward functions in algorithmic trading heavily rely on expert knowledge, posing challenges in their design and implementation. To tackle this, the reward-driven double DQN (R-DDQN) algorithm is proposed, integrating human feedback via a reward function network trained on expert demonstrations. Additionally, a classification-based training method is employed for optimizing the reward function network. The experiments, conducted on datasets including HSI, IXIC, SP500, GOOGL, MSFT, and INTC, show that the proposed method outperforms all baselines across six datasets and achieves a maximum cumulative return of 1502% within 24 months. [ABSTRACT FROM AUTHOR]

Background: The nucleus accumbens (NAc) is a key node of the brain reward circuit driving reward-related behavior. Dysregulation of NAc has been demonstrated to contribute to pathological markers of addiction in substance use disorder (SUD) making it a potential therapeutic target for brain stimulation. Transcranial focused ultrasound (tFUS) is an emerging non-invasive brain stimulation approach that can modulate deep brain regions with a high spatial resolution. However, there is currently no evidence showing how the brain activity of NAc and brain functional connectivity within the reward network neuromodulated by tFUS on the NAc. Methods: In this pilot study, we carried out a single-blind, sham-controlled clinical trial using functional magnetic resonance imaging (fMRI) to investigate the underlying mechanism of tFUS neuromodulating the reward network through NAc in ten healthy adults. Specifically, the experiment consists of a 20- min concurrent tFUS/fMRI scan and two 24-min resting-state fMRI before and after the tFUS session. Results: Firstly, our results demonstrated the feasibility and safety of 20-min tFUS on NAc. Additionally, our findings demonstrated that bilateral NAc was inhibited during tFUS on the left NAc compared to sham. Lastly, increased functional connectivity between the NAc and medial prefrontal cortex (mPFC) was observed after tFUS on the left NAc, but no changes for the sham group. Conclusion: Delivering tFUS to the NAc can modulate brain activations and functional connectivity within the reward network. These preliminary findings suggest that tFUS could be potentially a promising neuromodulation tool for the direct and non-invasive management of the NAc and shed new light on the treatment for SUD and other brain diseases that involve reward processing. [ABSTRACT FROM AUTHOR]

Auditory verbal hallucinations (AVHs) in schizophrenia is proved to be associated with dysfunction of mesolimbic-cortical circuits, especially during abnormal salient and internal verbal resource monitoring processing procedures. However, the information flow among areas involved in coordinated interaction implicated the pathophysiology of AVHs remains unclear. We used spectral dynamic causal modeling (DCM) to quantify connections among eight critical hubs of reward network in 86 first-episode drug-naïve schizophrenia patients with AVHs (AVH), 93 patients without AVHs (NAVH), and 88 matched normal controls (NC) using resting-state functional magnetic resonance imaging. Group-level connection coefficients, between-group differences and correlation analysis between image measures and symptoms were performed. DCM revealed weaker effective connectivity (EC) from right ventral striatum (RVS) to ventral tegmental area (VTA) in AVH compared to NAVH. AVH showed stronger EC from left anterior insula (AI) to RVS, stronger EC from RVS to anterior cingulate cortex (ACC), and stronger EC from VTA to posterior cingulate cortex (PCC) compared to NC. The correlation analysis results were mostly visible in the negative correlation between EC from right AI to ACC and positive sub-score, P1 sub-score, and P3 sub-score of PNASS in group-level. These findings suggest that neural causal interactions between the reward network associated with AVHs are disrupted, expanding the evidence for potential neurobiological mechanisms of AVHs. Particularly, dopamine-dependent salience attribution and top-down monitoring impairments and compensatory effects of enhanced excitatory afferents to ACC, which may provide evidence for a therapeutic target based on direct in vivo of AVHs in schizophrenia. [ABSTRACT FROM AUTHOR]

The social motivation hypothesis proposes that the social deficits of autism spectrum disorder (ASD) are related to reward system dysfunction. However, functional connectivity (FC) patterns of the reward network in ASD have not been systematically explored yet. The reward network was defined as eight regions of interest (ROIs) per hemisphere, including the nucleus accumbens (NAc), caudate, putamen, anterior cingulate cortex (ACC), ventromedial prefrontal cortex (vmPFC), orbitofrontal cortex (OFC), amygdala, and insula. We computed both the ROI-wise resting-state FC and seed-based whole-brain FC in 298 ASD participants and 348 typically developing (TD) controls from the Autism Brain Imaging Data Exchange I dataset. Two-sample t -tests were applied to obtain the aberrant FCs. Then, the association between aberrant FCs and clinical symptoms was assessed with Pearson's correlation or Spearman's correlation. In addition, Neurosynth Image Decoder was used to generate word clouds verifying the cognitive functions of the aberrant pathways. Furthermore, a three-way multivariate analysis of variance (MANOVA) was conducted to examine the effects of gender, subtype and age on the atypical FCs. For the within network analysis, the left ACC showed weaker FCs with both the right amygdala and left NAc in ASD compared with TD, which were negatively correlated with the Autism Diagnostic Observation Schedule (ADOS) total scores and Social Responsiveness Scale (SRS) total scores respectively. For the whole-brain analysis, weaker FC (i.e., FC between the left vmPFC and left calcarine gyrus, and between the right vmPFC and left precuneus) accompanied by stronger FC (i.e., FC between the left caudate and right insula) were exhibited in ASD relative to TD, which were positively associated with the SRS motivation scores. Additionally, we detected the main effect of age on FC between the left vmPFC and left calcarine gyrus, of subtype on FC between the right vmPFC and left precuneus, of age and age-by-gender interaction on FC between the left caudate and right insula. Our findings highlight the crucial role of abnormal FC patterns of the reward network in the core social deficits of ASD, which have the potential to reveal new biomarkers for ASD. • Systematic exploring of reward network's abnormal functional connectivity (FC) patterns in autism spectrum disorder (ASD) • Evaluating the effects of gender, subtype and age on the abnormal FC • Analysis based on a large-scale multi-site dataset ensures the reliability of the findings • Reduced anterior cingulate cortex-limbic, decreased anterior-posterior, and enhanced caudate-insula FC were revealed in ASD [ABSTRACT FROM AUTHOR]

Anhedonia is a significant predictor of disease progression and treatment outcomes in Major Depressive Disorder (MDD), linked to reward network dysfunctions. However, understanding of its underlying neural mechanisms remains limited. This study aimed to investigate the brain functional mechanisms underlying MDD with anhedonia using resting-state functional magnetic resonance imaging (rs-fMRI). The Snaith-Hamilton Pleasure Scale (SHAPS) was used to evaluation MDD with anhedonia (anMDD) and non-anhedonia MDD (non-anMDD). Forty-eight patients with anMDD, Forty-four patients with non-anMDD, and Fifty healthy controls (HCs) were enrolled for the fMRI scans. A seed-based functional connectivity (FC) method was employed to explore reward network abnormalities. anMDD patients exhibited lower FC values in Ventral Striatum (VS), right lateral Ventral Tegmental Area (VTA_R), left Thalamus (THA_L), and higher FC values in Ventromedial Prefrontal Cortex (vmPFC), left Anterior Insula (AI_L), and Presupplementary Motor Area (Pre-SMA) compared to HCs. Comparing anMDD to non-anMDD, significant differences were observed in FC values of VS, vmPFC, Pre-SMA, and THA_L regions. Correlation analysis revealed positive correlations between FC values of VS_R and NAc_R, as well as THA_L and Cerebellum_Crus1_L, with SHAPS scores. Negative correlations were observed between FC values of Pre-SMA and the right caudate, and between vmPFC and Frontal_Mid_Orb_L, and SHAPS scores. Both anMDD and non-anMDD groups demonstrated abnormal FCs in the reward network. These findings indicate distinct roles of reward-related circuits in the two subtypes, contributing to a refined understanding of depression phenotypes and potential directions for targeted interventions. • MDD is globally debilitating, diagnostic heterogeneity is crucial for current challenges in diagnosis and treatment. • Anhedonia is a core MDD symptom. • Reward-related circuits have distinct roles in MDD and non-MDD. [ABSTRACT FROM AUTHOR]

Chronic insomnia disorder (CID) is frequently comorbid with depression, and both conditions are believed to involve disruptions in the reward network. However, the potential effects of genetic polymorphisms in modulating this network remain largely unexplored. In this study, we recruited 50 CID patients with high (CID-HD) and low (CID-LD) depressive symptoms and assessed their reward networks using resting-state functional MRI. Additionally, we calculated the multilocus genetic profile score (MGPS) to examine the influence of depression and dopamine genetic variation on the nucleus accumbens functional connectivity (NAFC) network in CID patients. Although the MGPS did not show a significant difference between the two CID groups, its influence on the NAFC network was observed in the salience network (SN) and visual network (VN) in CID patients. When comparing CID-HD patients to CID-LD patients, we found that CID-HD patients exhibited decreased NAFC in the internal reward network, default mode network, SN, and sensorimotor network, while showing increased NAFC in the executive control network (ECN) and VN. Furthermore, the influence of MGPS on the reward network was only significant in CID-HD patients, specifically in the internal reward network and ECN. These findings suggest that genetic variations related to dopamine may modulate the reward network differently in CID patients with and without depressive symptoms. These results contribute to our understanding of the pathophysiology of polygenic effects underlying brain network abnormalities in CID patients with depression. • This study investigates the cumulative DA genetic effect on the reward network in individuals with insomnia and depression. • Insomnia patients with depression shown disrupted reward network including the DMN, SN, and SMN. • DA-related genetic variations have a specific impact on the reward network in insomnia patients with comorbid depression. [ABSTRACT FROM AUTHOR]

Major depressive disorder (MDD) represents a serious public health concern, negatively affecting individuals' quality of life and making a substantial contribution to the global burden of disease. Anhedonia is a core symptom of MDD and is associated with poor treatment outcomes. Variability in anhedonia components within MDD has been observed, suggesting heterogeneity in psychopathology across subgroups. However, little is known about anhedonia subgroups in MDD and their underlying neural correlates across subgroups. To address this question, we employed a hierarchical cluster analysis based on Temporal Experience of Pleasure Scale subscales in 60 first-episode, drug-naive MDD patients and 32 healthy controls. Then we conducted a connectome-wide association study and whole-brain voxel-wise functional analyses for identified subgroups. There were three main findings: (1) three subgroups with different anhedonia profiles were identified using a data mining approach; (2) several parts of the reward network (especially pallidum and dorsal striatum) were associated with anticipatory and consummatory pleasure; (3) different patterns of within- and between-network connectivity contributed to the disparities of anhedonia profiles across three MDD subgroups. Here, we show that anhedonia in MDD is not uniform and can be categorized into distinct subgroups, and our research contributes to the understanding of neural underpinnings, offering potential treatment directions. This work emphasizes the need for tailored approaches in the complex landscape of MDD. The identification of homogeneous, stable, and neurobiologically valid MDD subtypes could significantly enhance our comprehension and management of this multifaceted condition. [ABSTRACT FROM AUTHOR]

The human reward network consists of interconnected brain regions that process stimuli associated with satisfaction and modulate pleasure-seeking behaviors. Impairments in reward processing have been implicated in several medical and psychiatric conditions, and there is a growing interest in disentangling the underlying pathophysiological mechanisms. The brain–gut axis plays a regulatory role in several higher-order neurophysiological pathways, including reward processing. In this context, the aim of the current review was to critically appraise research findings on the contribution of the brain–gut axis to the human reward system. Enteric neuropeptides, which are implicated in the regulation of hunger and satiety, such as ghrelin, PYY3–36, and glucagon-like peptide 1 (GLP-1), have been associated with the processing of food-related, alcohol-related, and other non-food-related rewards, maintaining a delicate balance between the body’s homeostatic and hedonic needs. Furthermore, intestinal microbiota and their metabolites have been linked to differences in the architecture and activation of brain reward areas in obese patients and patients with attention deficit and hyperactivity disorder. Likewise, bariatric surgery reduces hedonic eating by altering the composition of gut microbiota. Although existing findings need further corroboration, they provide valuable information on the pathophysiology of reward-processing impairments and delineate a novel framework for potential therapeutic interventions.

Individuals with schizophrenia (SZ) show impairment in social functioning. The reward network and the emotional salience network are considered to play important roles in social interaction. The current study investigated alterations in the resting-state (rs-) amplitude of low-frequency fluctuation (ALFF), fractional ALFF (fALFF), regional homogeneity (ReHo) and functional connectivity (fc) in the reward network and the emotional salience network in SZ patients. MRI scans were collected from 60 subjects, including 30 SZ patients and 30 matched healthy controls. SZ symptoms were measured using the Positive and Negative Syndrome Scale (PANSS). We analyzed the ALFF, fALFF and ReHo in key brain regions in the reward network and emotional salience network as well as rs-fc among the bilateral amygdala, lateral orbitofrontal cortex (OFC), medial OFC and insula between groups. The SZ patients demonstrated increased ALFF in the right caudate and right putamen, increased fALFF and ReHo in the bilateral caudate, putamen and pallidum, along with decreased fALFF in the bilateral insula. Additionally, reduced rs-fc was found between the right lateral OFC and the left amygdala, which simultaneously belong to the reward network and the emotional salience network. These findings highlight the association between impaired social functioning in SZ patients and aberrant resting-state ALFF, fALFF, ReHo and fc. Future studies are needed to conduct network-based statistical analysis and task-state fMRI, reflecting live social interaction to advance our understanding of the mechanism of social interaction deficits in SZ. [ABSTRACT FROM AUTHOR]

Introduction: Oxytocin (OXT) is proposed as a potential therapeutic peptide for social dysfunction due to its modulatory actions on socioemotional regulation in humans. While the majority of studies have used intranasal OXT administration, we have recently shown that oral (lingual spray), but not intranasal, administration can significantly enhance activity of the brain reward system in response to emotional faces in males; however, its effects on females are unknown. Methods: Seventy healthy females participated in the current randomized, placebo-controlled, pharmaco-imaging clinical trial, and the results were compared with our previous data from 75 males who underwent the same protocol. Participants were randomly assigned to OXT (24 IU) or placebo (PLC) groups and completed an implicit emotional face paradigm (angry/fear/happy/neutral) where they were only required to identify face gender. Results: In line with previous results in males, oral OXT significantly increased plasma OXT concentration changes and enhanced putamen responses to all emotional faces compared to PLC in females. Additionally, OXT increased left amygdala activity to happy and angry faces and enhanced putamen-superior temporal gyrus functional coupling during processing of happy faces in females which was significantly different from males. Conclusion: Our findings suggest that oral OXT enhances responses in both reward and emotional-processing networks in females as well as males, and additionally, in females, it strengthens coupling between reward and social cognition regions. [ABSTRACT FROM AUTHOR]

Algorithmic trading is playing an increasingly important role in the financial market, achieving more efficient trading strategies by replacing human decision-making. Among numerous trading algorithms, deep reinforcement learning is gradually replacing traditional high-frequency trading strategies and has become a mainstream research direction in the field of algorithmic trading. This paper introduces a novel approach that leverages reinforcement learning with human feedback (RLHF) within the double DQN algorithm. Traditional reward functions in algorithmic trading heavily rely on expert knowledge, posing challenges in their design and implementation. To tackle this, the reward-driven double DQN (R-DDQN) algorithm is proposed, integrating human feedback via a reward function network trained on expert demonstrations. Additionally, a classification-based training method is employed for optimizing the reward function network. The experiments, conducted on datasets including HSI, IXIC, SP500, GOOGL, MSFT, and INTC, show that the proposed method outperforms all baselines across six datasets and achieves a maximum cumulative return of 1502% within 24 months.

Dandan Li,1– 3,* Long Zhang,4,* Tongjian Bai,4,* Bensheng Qiu,5 Chunyan Zhu,1– 3 Kai Wang1,2,4,6,7 1School of Mental Health and Psychological Sciences, Anhui Medical University, Hefei, People’s Republic of China; 2Institute of Artificial Intelligence, Hefei Comprehensive National Science Center, Hefei, People’s Republic of China; 3Research Center for Translational Medicine, Second Hospital of Anhui Medical University, Hefei, People’s Republic of China; 4Department of Neurology, First Affiliated Hospital of Anhui Medical University, Hefei, People’s Republic of China; 5Hefei National Laboratory for Physical Sciences at the Microscale and the Centers for Biomedical Engineering, University of Science and Technology of China., Hefei, People’s Republic of China; 6Anhui Province Key Laboratory of Cognition and Neuropsychiatric Disorders, Hefei, People’s Republic of China; 7Collaborative Innovation Center of Neuropsychiatric Disorders and Mental Health, Hefei, People’s Republic of China*These authors contributed equally to this workCorrespondence: Chunyan Zhu; Kai Wang, Email ayswallow@126.com; wangkai1964@126.comIntroduction: Empathy traits are highly heritable and linked with reward processing. It is implicated that common variations of the oxytocin-receptor gene (OXTR) play a modulatory effect on empathic performance. However, it is unclear about the neural substrates underlying the modulatory effect of the OXTR genotype on empathic performance. This study aimed to characterize the modulatory effect of common OXTR variations on reward-circuitry function and its relationship with empathy.Methods: Based on the seed of the nucleus accumbens (NAcc; a key hub of reward circuitry), we examined differences in spontaneous local activity and functional connectivity between OXTR rs2268493 genotype groups and their relationship with empathic performance among 402 high-homogeneity participants.Results: Comparing with C carriers (CC/CT) group, the individuals with the rs2268493 TT genotype exhibited lower functional connectivity of the right NAcc with the medial prefrontal cortex (mPFC) and inferior frontal gyrus. Similarly lower functional connectivity was found between the left NAcc and mPFC. Consequently, no significant difference was found in the spontaneous local activity of NAcc.Discussion: Our findings suggested that common OXTR variations have a modulatory effect on the connection of the NAcc with the hub of empathic networks (mPFC and IFG), which may provide insight on the neural substrate underlying the modulatory effect of OXTR on empathic behavior.Keywords: empathy, oxytocin-receptor gene, reward network, RS-fMRI, rs2268493

Individuals with schizophrenia (SZ) show impairment in social functioning. The reward network and the emotional salience network are considered to play important roles in social interaction. The current study investigated alterations in the resting-state (rs-) amplitude of low-frequency fluctuation (ALFF), fractional ALFF (fALFF), regional homogeneity (ReHo) and functional connectivity (fc) in the reward network and the emotional salience network in SZ patients. MRI scans were collected from 60 subjects, including 30 SZ patients and 30 matched healthy controls. SZ symptoms were measured using the Positive and Negative Syndrome Scale (PANSS). We analyzed the ALFF, fALFF and ReHo in key brain regions in the reward network and emotional salience network as well as rs-fc among the bilateral amygdala, lateral orbitofrontal cortex (OFC), medial OFC and insula between groups. The SZ patients demonstrated increased ALFF in the right caudate and right putamen, increased fALFF and ReHo in the bilateral caudate, putamen and pallidum, along with decreased fALFF in the bilateral insula. Additionally, reduced rs-fc was found between the right lateral OFC and the left amygdala, which simultaneously belong to the reward network and the emotional salience network. These findings highlight the association between impaired social functioning in SZ patients and aberrant resting-state ALFF, fALFF, ReHo and fc. Future studies are needed to conduct network-based statistical analysis and task-state fMRI, reflecting live social interaction to advance our understanding of the mechanism of social interaction deficits in SZ.

Stroke survivors not only suffer from severe motor, speech and neurocognitive deficits, but in many cases also from a “lack of pleasure” and a reduced motivational level. Especially apathy and anhedonic symptoms can be linked to a dysfunction of the reward system. Rewards are considered as important co-factor for learning, so the question arises as to why and how this affects the rehabilitation of stroke patients.We investigated reward behaviour, learning ability and brain network connectivity in acute (3-7d) mild to moderate stroke patients (n = 28) and age-matched healthy controls (n = 26). Reward system activity was assessed using the Monetary Incentive Delay task (MID) during magnetoencephalography (MEG). Coherence analyses were used to demonstrate reward effects on brain functional network connectivity.The MID-task showed that stroke survivors had lower reward sensitivity and required greater monetary incentives to improve performance and showed deficits in learning improvement. MEG-analyses showed a reduced network connectivity in frontal and temporoparietal regions. All three effects (reduced reward sensitivity, reduced learning ability and altered cerebral connectivity) were found to be closely related and differed strongly from the healthy group.Our results reinforce the notion that acute stroke induces reward network dysfunction, leading to functional impairment of behavioural systems. These findings are representative of a general pattern in mild strokes and are independent of the specific lesion localisation. For stroke rehabilitation, these results represent an important point to identify the reduced learning capacity after stroke and to implement individualised recovery exercises accordingly.

Background: Tobacco addiction is a chronic, relapsing mental disorder characterized by compulsive tobacco seeking and smoking. Current evidence shows that tobacco addiction exerts their initial reinforcing effects by activating reward circuits in the brain, but the causal connectivity among reward circuits is still unclear. Therefore, it is vital to understand how the reward network works to lead to the compulsive smoking behaviour.Method: We applied dynamic causal modelling (DCM) to resting-state functional magnetic resonance (rs-fMRI) to characterize changes in effective connectivity (EC) among eight major hubs from reward network between 76 long-term male smokers and 55 nonsmoking volunteers (matched with age, gender and education).Results: Relative to the healthy controls, long-term smokers had stronger ECs from the right anterior insula to left ventral striatum, posterior cingulate cortex (PCC) to ventral tegmental area (VTA), PCC to left anterior insula, left anterior insula to VTA, and ventromedial prefrontal cortex (vmPFC) to PCC and weaker ECs from the VTA to left ventral striatum, right anterior insula to right ventral striatum, and anterior cingulate cortex (ACC) to right anterior insula.Conclusions: Overall, our findings revealed disrupted neural causal interactions among parts of the reward network associated with tobacco addiction, expanding the growing evidence for the potential neurobiological mechanisms of tobacco addiction. We found abnormalities within the mesocorticolimbic system and a top-down regulation disorder in the dopamine-dependent process of response inhibition and salience attribution among long-term smokers, which may facilitate the development of effective therapies in tobacco addiction. [ABSTRACT FROM AUTHOR]

Different acupoints exhibiting similar therapeutic effects are a common phenomenon in acupuncture clinical practice. However, the mechanism underlying this phenomenon remains unclear. This study aimed to investigate the similarities and differences in cerebral activities elicited through stimulation of CV12 and ST36, the two most commonly used acupoints, in the treatment of gastrointestinal diseases, so as to partly explore the mechanism of the different acupoints with similar effects. Thirty-eight eligible functional dyspepsia (FD) patients were randomly assigned into either group A (CV12 group) or group B (ST36 group). Each patient received five acupuncture treatments per week for 4 weeks. The Symptom Index of Dyspepsia (SID), Nepean Dyspepsia Symptom Index (NDSI), and Nepean Dyspepsia Life Quality Index (NDLQI) were used to assess treatment efficacy. Functional MRI (fMRI) scans were performed to detect cerebral activity changes at baseline and at the end of the treatment. The results demonstrated that (1) improvements in NDSI, SID, and NDLQI were found in both group A and group B (p < 0.05). However, there were no significant differences in the improvements of the SID, NDSI, and NDLQI scores between group A and group B (p > 0.05); (2) all FD patients showed significantly increased amplitude of low-frequency fluctuation (ALFF) in the left postcentral gyrus after acupuncture treatment, and the changes of ALFF in the left postcentral gyrus were significantly related to the improvements of SID scores (r = 0.358, p = 0.041); and (3) needling at CV12 significantly decreased the resting-state functional connectivity (rsFC) between the left postcentral gyrus and angular gyrus, caudate, middle frontal gyrus (MFG), and cerebellum, while needling at ST36 significantly increased the rsFC between the left postcentral gyrus with the precuneus, superior frontal gyrus (SFG), and MFG. The results indicated that CV12 and ST36 shared similar therapeutic effects for dyspepsia, with common modulation on the activity of the postcentral gyrus in FD patients. However, the modulatory pattern on the functional connectivity of the postcentral gyrus was different. Namely, stimulation of CV12 primarily involved the postcentral gyrus–reward network, while stimulation of ST36 primarily involved the postcentral gyrus–default mode network circuitry. [ABSTRACT FROM AUTHOR]

Different acupoints exhibiting similar therapeutic effects are a common phenomenon in acupuncture clinical practice. However, the mechanism underlying this phenomenon remains unclear. This study aimed to investigate the similarities and differences in cerebral activities elicited through stimulation of CV12 and ST36, the two most commonly used acupoints, in the treatment of gastrointestinal diseases, so as to partly explore the mechanism of the different acupoints with similar effects. Thirty-eight eligible functional dyspepsia (FD) patients were randomly assigned into either group A (CV12 group) or group B (ST36 group). Each patient received five acupuncture treatments per week for 4 weeks. The Symptom Index of Dyspepsia (SID), Nepean Dyspepsia Symptom Index (NDSI), and Nepean Dyspepsia Life Quality Index (NDLQI) were used to assess treatment efficacy. Functional MRI (fMRI) scans were performed to detect cerebral activity changes at baseline and at the end of the treatment. The results demonstrated that (1) improvements in NDSI, SID, and NDLQI were found in both group A and group B (p < 0.05). However, there were no significant differences in the improvements of the SID, NDSI, and NDLQI scores between group A and group B (p > 0.05); (2) all FD patients showed significantly increased amplitude of low-frequency fluctuation (ALFF) in the left postcentral gyrus after acupuncture treatment, and the changes of ALFF in the left postcentral gyrus were significantly related to the improvements of SID scores (r = 0.358, p = 0.041); and (3) needling at CV12 significantly decreased the resting-state functional connectivity (rsFC) between the left postcentral gyrus and angular gyrus, caudate, middle frontal gyrus (MFG), and cerebellum, while needling at ST36 significantly increased the rsFC between the left postcentral gyrus with the precuneus, superior frontal gyrus (SFG), and MFG. The results indicated that CV12 and ST36 shared similar therapeutic effects for dyspepsia, with common modulation on the activity of the postcentral gyrus in FD patients. However, the modulatory pattern on the functional connectivity of the postcentral gyrus was different. Namely, stimulation of CV12 primarily involved the postcentral gyrus–reward network, while stimulation of ST36 primarily involved the postcentral gyrus–default mode network circuitry.

Previous research has shown that acute sleep deprivation can influence the reward networks. However, it is unclear whether and how the intrinsic reward network is altered in chronic insomnia disorder (CID). In the present study, we aimed to investigate whether the reward network is altered in patients with CID using resting-state functional magnetic resonance imaging (fMRI) data. Forty-two patients with CID and 33 healthy controls (HCs) were enrolled and underwent resting-state fMRI. Nucleus accumbens (NAc) - based functional connectivity (NAFC) was evaluated to explore the differences in the reward network between the CID and HC groups. Pearson correlation analysis was used to evaluate the clinical significance of altered NAFC networks. Compared to those in the HC group, increased NAFC was found in the salience and limbic networks, while decreased NAFC was found in the default mode network (DMN) and within the reward circuit in patients with CID. In addition, decreased FC between the NAc and DMN was associated with insomnia severity, while NAFC within the reward network was associated with depression symptoms in patients with CID. These findings showed that the reward network is dysfunctional and associated with depression symptom in patients with CID. Future studies of CID should consider both insomnia and depression symptoms to disentangle the role of insomnia and depression in the relationship under study. [ABSTRACT FROM AUTHOR]

Gender roles are anti-dichotomous and malleable social constructs that should theoretically be constructed independently from biological sex. However, it is unclear whether and how the factor of sex is related to neural mechanisms involved in social constructions of gender roles. Thus, the present study aimed to investigate sex specificity in gender role constructions and the corresponding underlying neural mechanisms. We measured gender role orientation using the Bem Sex-Role Inventory, used a voxel-based global brain connectivity method based on resting-state functional magnetic resonance imaging to characterize the within-network connectivity in the brain reward network, and analyzed how the integration of the reward network is related to gender role scores between sex groups. An omnibus analysis of voxel-wise global brain connectivity values within a two-level linear mixed model revealed that in female participants, femininity scores were positively associated with integration in the posterior orbitofrontal cortex and subcallosal cortex, whereas masculinity scores were positively associated with integration in the frontal pole. By contrast, in male participants, masculinity was negatively correlated with integration in the nucleus accumbens and subcallosal cortex. For the first time, the present study revealed the sex-specific neural mechanisms underlying distinct gender roles, which elucidates the process of gender construction from the perspective of the interaction between reward sensitivity and social reinforcement.

Gender roles are anti-dichotomous and malleable social constructs that should theoretically be constructed independently from biological sex. However, it is unclear whether and how the factor of sex is related to neural mechanisms involved in social constructions of gender roles. Thus, the present study aimed to investigate sex specificity in gender role constructions and the corresponding underlying neural mechanisms. We measured gender role orientation using the Bem Sex-Role Inventory, used a voxel-based global brain connectivity method based on resting-state functional magnetic resonance imaging to characterize the within-network connectivity in the brain reward network, and analyzed how the integration of the reward network is related to gender role scores between sex groups. An omnibus analysis of voxel-wise global brain connectivity values within a two-level linear mixed model revealed that in female participants, femininity scores were positively associated with integration in the posterior orbitofrontal cortex and subcallosal cortex, whereas masculinity scores were positively associated with integration in the frontal pole. By contrast, in male participants, masculinity was negatively correlated with integration in the nucleus accumbens and subcallosal cortex. For the first time, the present study revealed the sex-specific neural mechanisms underlying distinct gender roles, which elucidates the process of gender construction from the perspective of the interaction between reward sensitivity and social reinforcement. [ABSTRACT FROM AUTHOR]

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Chronic low back pain (cLBP) is a prevalent disorder. A growing body of evidence linking the pathology of the reward network to chronic pain suggests that pain sensitization may contribute to cLBP chronification via disruptions of mesocortical and mesolimbic circuits in the reward system. Resting-state (RS) functional magnetic resonance imaging (fMRI) data was acquired from 90 patients with cLBP and 74 matched pain-free controls (HCs) at baseline and after a manipulation for back pain intensification. The ventral tegmental area (VTA) was chosen as a seed region to perform RS functional connectivity (FC) analysis. Baseline rsFC of both the mesocortical (between the VTA and bilateral rostral anterior cingulate cortex (rACC)/and medial prefrontal cortex (mPFC)) and mesolimbic (between the VTA and bilateral hippocampus/parahippocampus) pathways was reduced in patients with cLBP (vs. HCs). In addition, patients exhibiting higher back pain intensity (compared to the relatively lower back pain intensity condition) also showed increases in both mesocortical and mesolimbic connectivity, implicating these pathways in pain downregulation in cLBP. Mediation analysis further isolated the mesolimbic (VTA-hippocampus/parahippocampus) dysconnectivity as a neural mechanism mediating the association between mechanical pain sensitivity (indexed by P40 pressure) and cLBP severity. In sum, the current study demonstrates deficient mesocorticolimbic connectivity in cLBP, with mesolimbic dysconnectivity potentially mediating the contribution of pain sensitization to pain chronification. These reward network dysfunctions and purportedly, dopaminergic dysregulations, may help us to identify key brain targets of neuromodulation in the treatment of cLBP.

Professional pride is a positive emotion that includes self-reflection or evaluation and attitude toward one’s own occupational group. Uniforms can encourage the wearer to have professional pride. The current study aimed to elucidate the neural basis of professional pride using an experimental task related to the self in uniform and functional magnetic resonance imaging (fMRI). The person-adjective matching task, in which a participant or other in uniform or casual wear was presented with positive and negative words, was used for scanning fMRI. Imaging data from 21 adults who had an occupation requiring a uniform were analyzed to identify the main and interaction effects of individual (self vs. other), clothes (uniform vs. casual wear), and valence (positive vs. negative). Identified brain activities were correlated with psychological scales including the Rosenberg Self-esteem Scale and Group Environment Questionnaire. Whole brain analyses found that the interaction between individual and clothes was present in multiple regions such as the right ventrolateral prefrontal cortex (VLPFC), left dorsolateral prefrontal cortex, left middle and inferior temporal gyri, left posterior superior temporal sulcus, right temporoparietal junction, left lingual gyrus, left calcarine cortex, right insula, left caudate, and right putamen. In particular, activities in the right VLPFC, left calcarine cortex, and right putamen in the self/uniform condition were positively correlated with several psychological scales. These results suggest that professional pride may be represented through multiple brain networks related to empathy, reward, and emotion regulation as well as the theory-of-mind network. The neural basis of professional pride is closely related to positive self-evaluation and group cohesion.

Professional pride is a positive emotion that includes self-reflection or evaluation and attitude toward one's own occupational group. Uniforms can encourage the wearer to have professional pride. The current study aimed to elucidate the neural basis of professional pride using an experimental task related to the self in uniform and functional magnetic resonance imaging (fMRI). The person-adjective matching task, in which a participant or other in uniform or casual wear was presented with positive and negative words, was used for scanning fMRI. Imaging data from 21 adults who had an occupation requiring a uniform were analyzed to identify the main and interaction effects of individual (self vs. other), clothes (uniform vs. casual wear), and valence (positive vs. negative). Identified brain activities were correlated with psychological scales including the Rosenberg Self-esteem Scale and Group Environment Questionnaire. Whole brain analyses found that the interaction between individual and clothes was present in multiple regions such as the right ventrolateral prefrontal cortex (VLPFC), left dorsolateral prefrontal cortex, left middle and inferior temporal gyri, left posterior superior temporal sulcus, right temporoparietal junction, left lingual gyrus, left calcarine cortex, right insula, left caudate, and right putamen. In particular, activities in the right VLPFC, left calcarine cortex, and right putamen in the self/uniform condition were positively correlated with several psychological scales. These results suggest that professional pride may be represented through multiple brain networks related to empathy, reward, and emotion regulation as well as the theory-of-mind network. The neural basis of professional pride is closely related to positive self-evaluation and group cohesion. [ABSTRACT FROM AUTHOR]

Converging evidence points to the crucial role of brain connectivity involved in aberrant behavioral control and reward reactivity in the onset and maintenance of binge eating. However, the directional interaction pattern between brain's reward and inhibitory control systems in people with binge eating episodes is largely unknown. Resting-state fMRI data were collected from 36 adults with binge eating episodes (age: 19.05 ± 0.90) and 36 well-matched controls (age: 18.88 ± 0.78). We applied spectral dynamic causal modeling approach to estimate effective connectivity of the executive control network (ECN) and reward network (RN) with 15 predefined regions of interest, and investigate the between-group differences in directional connectivity. Compared with controls, the positive connections within the ECN were significantly strengthened in individuals with binge eating episodes, while the negative connections from the ECN to RN and from the RN to ECN were significantly weakened. In adults with binge eating episodes, the RN→ECN connectivity was positively related to binge frequency even controlling for age, sex, and body mass index. This study represents an important first step in addressing the role of directional integration between reward and inhibitory control networks in binge eating, and provides novel evidence that the ability of people with binge eating episodes to maintain a balance between inhibitory control and reward reactivity is decreased, as reflected by diminished bidirectional negative effects of prefrontal-subcortical circuitry at rest. • This study examined the altered directional interaction between reward and inhibitory control networks in people with binge eating episodes using spectral dynamic causal modeling. • Compared with controls, the positive connections within the executive control network were significantly strengthened in adults with binge eating episodes, while the negative connections from the executive control network to reward network and from the reward network to executive control network were significantly weakened. • This study provides novel evidence that the ability of people with binge eating episodes to maintain a balance between inhibitory control and reward reactivity is decreased, as reflected by diminished bidirectional negative effects of prefrontal-subcortical circuitry at rest. [ABSTRACT FROM AUTHOR]

Baclofen, a GABA-B receptor agonist, is a promising treatment for alcohol use disorder (AUD). Its mechanism of action in this condition is unknown. GABA-B receptors interact with many biological systems potentially involved in AUD, including transduction pathways and neurotransmitter systems. Preclinical studies have shown that GABA-B receptors are involved in memory storage and retrieval, reward, motivation, mood and anxiety; neuroimaging studies in humans show that baclofen produces region-specific alterations in cerebral activity; GABA-B receptor activation may have neuroprotective effects; baclofen also has anti-inflammatory properties that may be of interest in the context of addiction. However, none of these biological effects fully explain the mechanism of action of baclofen in AUD. Data from clinical studies have provided a certain number of elements which may be useful for the comprehension of its mechanism of action: baclofen typically induces a state of indifference toward alcohol; the effective dose of baclofen in AUD is extremely variable from one patient to another; higher treatment doses correlate with the severity of the addiction; many of the side effects of baclofen resemble those of alcohol, raising the possibility that baclofen acts as a substitution drug; usually, however, there is no tolerance to the effects of baclofen during long-term AUD treatment. In the present article, the biological effects of baclofen are reviewed in the light of its clinical effects in AUD, assuming that, in many instances, clinical effects can be reliable indicators of underlying biological processes. In conclusion, it is proposed that baclofen may suppress the Pavlovian association between cues and rewards through an action in a critical part of the dopaminergic network (the amygdala), thereby normalizing the functional connectivity in the reward network. It is also proposed that this action of baclofen is made possible by the fact that baclofen and alcohol act on similar brain systems in certain regions of the brain.

Background: Alterations in the hedonic component of ingestive behaviors have been implicated as a possible risk factor in the pathophysiology of overweight and obese individuals. Neuroimaging evidence from individuals with increasing body mass index suggests structural, functional, and neurochemical alterations in the extended reward network and associated networks. Aim: To apply a multivariate pattern analysis to distinguish normal weight and overweight subjects based on gray and white-matter measurements. Methods: Structural images (N = 120, overweight N = 63) and diffusion tensor images (DTI) (N = 60, overweight N = 30) were obtained from healthy control subjects. For the total sample the mean age for the overweight group (females = 32, males = 31) was 28.77 years (SD = 9.76) and for the normal weight group (females = 32, males = 25) was 27.13 years (SD = 9.62). Regional segmentation and parcellation of the brain images was performed using Freesurfer. Deterministic tractography was performed to measure the normalized fiber density between regions. A multivariate pattern analysis approach was used to examine whether brain measures can distinguish overweight from normal weight individuals. Results: 1. White-matter classification: The classification algorithm, based on 2 signatures with 17 regional connections, achieved 97% accuracy in discriminating overweight individuals from normal weight individuals. For both brain signatures, greater connectivity as indexed by increased fiber density was observed in overweight compared to normal weight between the reward network regions and regions of the executive control, emotional arousal, and somatosensory networks. In contrast, the opposite pattern (decreased fiber density) was found between ventromedial prefrontal cortex and the anterior insula, and between thalamus and executive control network regions. 2. Gray-matter classification: The classification algorithm, based on 2 signatures with 42 morphological features, achieved 69% accuracy in discriminating overweight from normal weight. In both brain signatures regions of the reward, salience, executive control and emotional arousal networks were associated with lower morphological values in overweight individuals compared to normal weight individuals, while the opposite pattern was seen for regions of the somatosensory network. Conclusions: 1. An increased BMI (i.e., overweight subjects) is associated with distinct changes in gray-matter and fiber density of the brain. 2. Classification algorithms based on white-matter connectivity involving regions of the reward and associated networks can identify specific targets for mechanistic studies and future drug development aimed at abnormal ingestive behavior and in overweight/obesity.

Understanding the neural substrates of depression is crucial for diagnosis and treatment. Here, we review recent studies of functional and effective connectivity in depression, in terms of functional integration in the brain. Findings from these studies, including our own, point to the involvement of at least four networks in patients with depression. Elevated connectivity of a ventral limbic affective network appears to be associated with excessive negative mood (dysphoria) in the patients; decreased connectivity of a frontal‐striatal reward network has been suggested to account for loss of interest, motivation, and pleasure (anhedonia); enhanced default mode network connectivity seems to be associated with depressive rumination; and diminished connectivity of a dorsal cognitive control network is thought to underlie cognitive deficits especially ineffective top‐down control of negative thoughts and emotions in depressed patients. Moreover, the restoration of connectivity of these networks—and corresponding symptom improvement—following antidepressant treatment (including medication, psychotherapy, and brain stimulation techniques) serves as evidence for the crucial role of these networks in the pathophysiology of depression. [ABSTRACT FROM AUTHOR]

Baclofen, a GABA-B receptor agonist, is a promising treatment for alcohol use disorder (AUD). Its mechanism of action in this condition is unknown. GABA-B receptors interact with many biological systems potentially involved in AUD, including transduction pathways and neurotransmitter systems. Preclinical studies have shown that GABA-B receptors are involved in memory storage and retrieval, reward, motivation, mood and anxiety; neuroimaging studies in humans show that baclofen produces region-specific alterations in cerebral activity; GABA-B receptor activation may have neuroprotective effects; baclofen also has anti-inflammatory properties that may be of interest in the context of addiction. However, none of these biological effects fully explain the mechanism of action of baclofen in AUD. Data from clinical studies have provided a certain number of elements which may be useful for the comprehension of its mechanism of action: baclofen typically induces a state of indifference toward alcohol; the effective dose of baclofen in AUD is extremely variable from one patient to another; higher treatment doses correlate with the severity of the addiction; many of the side effects of baclofen resemble those of alcohol, raising the possibility that baclofen acts as a substitution drug; usually, however, there is no tolerance to the effects of baclofen during long-term AUD treatment. In the present article, the biological effects of baclofen are reviewed in the light of its clinical effects in AUD, assuming that, in many instances, clinical effects can be reliable indicators of underlying biological processes. In conclusion, it is proposed that baclofen may suppress the Pavlovian association between cues and rewards through an action in a critical part of the dopaminergic network (the amygdala), thereby normalizing the functional connectivity in the reward network. It is also proposed that this action of baclofen is made possible by the fact that baclofen and alcohol act on similar brain systems in certain regions of the brain. [ABSTRACT FROM AUTHOR]

The pretreatment neuroimaging markers from the resting-state brain network that could predict the early response to antidepressants are still unclear. The aim of the present study was to identify the performance of reward network features for discriminating patients with a dampened response to antidepressants. A total of 81 major depressive disorder (MDD) patients (44 patients with treatment-responsive depression (RD) and 37 patients with non-responding depression (NRD)) and 43 healthy controls (HC) underwent resting-state functional magnetic resonance imaging scans and clinical estimates. Bilateral nucleus accumbens (NAcc)-based networks were constructed for further functional connectivity (FC) analysis. The FC of the right superior frontal gyrus (SFG) (area under curve (AUC) = 0.837) and left parahippocampus (AUC = 0.770) within the left NAcc reward network, as well as the FC of the left SFG (AUC = 0.827) within the right NAcc reward network, could distinguish NRD subjects from RD subjects relatively well. Taken together, when considering the distinctive connectional pattern of the bilateral reward circuits, the synthetical differentiating effect was achieved to an optimal performance for discriminating NRD patients (AUC = 0.869), with balanced sensitivity (0.838) and specificity (0.818). The distinct pretreatment characteristics of the reward network make specific contributions to the early response to antidepressants and establish a promising imaging predictor for the classification of early efficacy. [ABSTRACT FROM AUTHOR]

Background and Objective: Several studies have shown that repetitive transcranial magnetic stimulation (rTMS), applied to the dorsolateral prefrontal cortex (DLPFC), can reduce cue-elicited craving in smokers. Currently, the mechanism of this effect is unknown. We used functional magnetic resonance imaging (fMRI) to explore the effect of a single treatment of rTMS on cortical and sub-cortical neural activity in non-treatment seeking nicotine-dependent participants.Methods: We conducted a randomized, counterbalanced, crossover trial in which participants attended two experimental visits separated by at least 1 week. On the first visit, participants received either active, or sham rTMS (10 Hz, 5 s-on, 10 s-off, 100% motor threshold, 3,000 pulses) over the left DLPFC, and on the second visit they received the opposite condition (active or sham). Cue craving fMRI scans were completed before and after each rTMS session.Results: A total of 11 non-treatment seeking nicotine-dependent cigarette smokers were enrolled in the study [six female, average age 39.7 ± 13.2, average cigarettes per day 17.3 ± 5.9]. Active rTMS decreased activity in the contralateral medial orbitofrontal cortex (mOFC) and ipsilateral nucleus accumbens (NAc) compared to sham rTMS.Conclusions: This preliminary data suggests that one session of rTMS applied to the DLPFC decreases brain activity in the NAc and mOFC in smokers.Scientific Significance: rTMS may exert its anti-craving effect by decreasing activity in the NAc and mOFC in smokers. Despite a small sample size, these findings warrant future rTMS/fMRI studies in addictions. (Am J Addict 2017;26:788-794). [ABSTRACT FROM AUTHOR]

Multiple genetic loci in the dopamine (DA) pathway have been associated with depression symptoms in patients with major depressive disorder (MDD). However, the neural mechanisms underlying the polygenic effects of the DA pathway on depression remain unclear. We used an imaging genetic approach to investigate the polygenic effects of the DA pathway on the reward network in MDD. Fifty-three patients and 37 cognitively normal (CN) subjects were recruited and underwent resting-state functional magnetic resonance imaging (R-fMRI) scans. Multivariate linear regression analysis was employed to measure the effects of disease and multilocus genetic profile scores (MGPS) on the reward network, which was constructed using the nucleus accumbens (NAc) functional connectivity (NAFC) network. DA-MGPS was widely associated within the NAFC network, mainly in the inferior frontal cortex, insula, hypothalamus, superior temporal gyrus, and occipital cortex. The pattern of DA-MGPS effects on the fronto-striatal pathway differed in MDD patients compared with CN subjects. More importantly, NAc-putamen connectivity mediates the association between DA MGPS and anxious depression traits in MDD patients. Our findings suggest that the DA multilocus genetic profile makes a considerable contribution to the reward network and anxious depression in MDD patients. These results expand our understanding of the pathophysiology of polygenic effects underlying brain network abnormalities in MDD.

The brain's reward network has been reported to be smaller in alcoholic men compared to nonalcoholic men, but little is known about the volumes of reward regions in alcoholic women. Morphometric analyses were performed on magnetic resonance brain scans of 60 long-term chronic alcoholics (ALC; 30 men) and 60 nonalcoholic controls (NC; 29 men). We derived volumes of total brain, and cortical and subcortical reward-related structures including the dorsolateral prefrontal (DLPFC), orbitofrontal, and cingulate cortices, and the temporal pole, insula, amygdala, hippocampus, nucleus accumbens septi (NAc), and ventral diencephalon (VDC). We examined the relationships of the volumetric findings to drinking history. Analyses revealed a significant gender interaction for the association between alcoholism and total reward network volumes, with ALC men having smaller reward volumes than NC men and ALC women having larger reward volumes than NC women. Analyses of a priori subregions revealed a similar pattern of reward volume differences with significant gender interactions for DLPFC and VDC. Overall, the volume of the cerebral ventricles in ALC participants was negatively associated with duration of abstinence, suggesting decline in atrophy with greater length of sobriety. [ABSTRACT FROM AUTHOR]

Recently, there has been renewed interest in the study of cognitive fatigue. It is known that fatigue is one of the most disabling symptoms in numerous neurological populations, including stroke, multiple sclerosis, Parkinson's disease, and traumatic brain injury. Behavioral studies of cognitive fatigue are hampered by lack of correlation of self-report measures with objective performance. Neuroimaging studies provide new insight about cognitive fatigue and its neural correlates. Impairment within the cortico-striatal network, involved in effort–reward calculation, has been suggested to be critically related to fatigue. The current review surveys the recent neuroimaging literature, and suggests promising avenues for future research. (JINS, 2013, 19, 1–5) [ABSTRACT FROM AUTHOR]

Parkinson's disease (PD) is associated with a number of behavioral disorders which may cause considerable social, professional or financial problems. Impulse control disorders (ICDs), such as pathological gambling, binge eating, compulsive shopping and hypersexuality occur in approximately 13-14% of PD patients. Further behavioral disorders are the dopamine dysregulation syndrome (DDS), a substance dependence characterized by craving for dopaminergic substances and punding (prolonged repetitive activities which are not goal-oriented). Treatment-related risk factors are dopamine agonists for ICDs and a high total dopaminergic dose for DDS and punding. Shared risk factors are young age at onset, impulsive personality traits, depression and possibly dyskinesia. At the neuronal level these behavioral disorders seem to be associated with changes in the reward system and dysfunction of the orbitofrontal cortex. The evidence level for management strategies is at present insufficient. For ICDs current clinical practice consists of discontinuation or reduction of dopamine agonists. [ABSTRACT FROM AUTHOR]

Identifying neuroimaging features to diagnose major depressive disorder (MDD) and predict treatment response remains challenging. Using the pretreatment dominant coactivation pattern (dCAP) analysis approach, we aimed to identify patients with MDD and predict antidepressant efficacy. Seventy-seven first-episode unmedicated MDD patients and forty-two age- and sex-matched healthy controls (HCs) were recruited in the study. The dCAP analysis was performed for the reward and default mode network (DMN) to identify the MDD patients from the HCs. The dCAP1 of the left posterior DMN and bilateral anterior DMN were significantly higher in the MDD group than in the HC group (P <.001), and the dCAP1 in the left posterior DMN was positively correlated with the baseline severity of depression (rho = 0.248, P =.030). Besides, the MDD group exhibited significantly higher dCAP1 in the right reward network than the HC group. Further correlation analyses revealed that the transfer probability in the right reward network was positively correlated with the treatment responsivity (r = 0.247, P =.030). Importantly, integrating the dCAPs of the above four subnetworks can effectively identify the patients with MDD (AUC = 0.920, P <.001). The distinct pretreatment features of the dCAP in the subnetwork of the DMN and reward network may serve as potential indicators for individual diagnosis and prediction of antidepressant response in the early stage. • Distinct features of dominant coactivation patterns were detected in depression; • The dCAP1 in the left posterior DMN was positively correlated with the baseline severity of depression; • The integrated dCAPs in four subnetworks can effectively identify patients with MDD. [ABSTRACT FROM AUTHOR]

Millions of women worldwide use oral contraceptives (OCs), often starting during puberty/adolescence. It is, however, unknown how OC use during this critical period of development affects the brain. The objective of the current study was to examine resting state functional connectivity (FC) in the default mode network (DMN), central executive network (CEN), salience network (SN), reward network (RN), and subcortical limbic network of the brain using independent component analysis (ICA) between pubertal- and adult-onset OC users (n = 27) and naturally cycling women (n = 48). It was hypothesized that OC use would result in network-specific increases and decreases in FC and that pubertal-onset OC use would result in differences to the aforementioned networks compared to adult-onset OC use. Pubertal-onset OC use is related to heightened FC in the SN compared to adult-onset OC users. In general, OC use also increases connectivity in the SN, CEN, RN, and subcortical limbic network compared to NC women. No significant differences in connectivity were observed in the DMN between OC users and NC women. These findings provide a mechanistic insight for the altered executive functioning and emotion/reward processing previously seen in OC users, which may then increase their vulnerability to mental health conditions. • OC use during puberty increases functional connectivity in the salience network. • OC use in general is related to more functional connectivity in the salience, central executive, and reward networks. • The higher functional connectivity in OC users provides mechanistic insight for altered cognition and mental health. [ABSTRACT FROM AUTHOR]

Chronic low back pain (cLBP) is a prevalent disorder. A growing body of evidence linking the pathology of the reward network to chronic pain suggests that pain sensitization may contribute to cLBP chronification via disruptions of mesocortical and mesolimbic circuits in the reward system. Resting-state (RS) functional magnetic resonance imaging (fMRI) data was acquired from 90 patients with cLBP and 74 matched pain-free controls (HCs) at baseline and after a manipulation for back pain intensification. The ventral tegmental area (VTA) was chosen as a seed region to perform RS functional connectivity (FC) analysis. Baseline rsFC of both the mesocortical (between the VTA and bilateral rostral anterior cingulate cortex (rACC)/and medial prefrontal cortex (mPFC)) and mesolimbic (between the VTA and bilateral hippocampus/parahippocampus) pathways was reduced in patients with cLBP (vs. HCs). In addition, patients exhibiting higher back pain intensity (compared to the relatively lower back pain intensity condition) also showed increases in both mesocortical and mesolimbic connectivity, implicating these pathways in pain downregulation in cLBP. Mediation analysis further isolated the mesolimbic (VTA-hippocampus/parahippocampus) dysconnectivity as a neural mechanism mediating the association between mechanical pain sensitivity (indexed by P40 pressure) and cLBP severity. In sum, the current study demonstrates deficient mesocorticolimbic connectivity in cLBP, with mesolimbic dysconnectivity potentially mediating the contribution of pain sensitization to pain chronification. These reward network dysfunctions and purportedly, dopaminergic dysregulations, may help us to identify key brain targets of neuromodulation in the treatment of cLBP. • Mesocortical and mesolimbic connectivity decreased in cLBP patients compared to controls. • Mesocortical and mesolimbic connectivity increased when back pain intensity increased. • Mesolimbic connectivity mediated the association between pain sensitivity and cLBP severity. [ABSTRACT FROM AUTHOR]

Chronic low back pain (cLBP) is a common disorder with unsatisfactory treatment options. Acupuncture has emerged as a promising method for treating cLBP. However, the mechanism underlying acupuncture remains unclear. In this study, we investigated the modulation effects of acupuncture on resting state functional connectivity (rsFC) of the periaqueductal gray (PAG) and ventral tegmental area (VTA) in patients with cLBP. Seventy-nine cLBP patients were recruited and assigned to four weeks of real or sham acupuncture. Resting state functional magnetic resonance imaging data were collected before the first and after the last treatment. Fifty patients completed the study. We found remission of pain bothersomeness in all treatment groups after four weeks, with greater pain relief after real acupuncture compared to sham acupuncture. We also found that real acupuncture can increase VTA/PAG rsFC with the amygdala, and the increased rsFC was associated with decreased pain bothersomeness scores. Baseline PAG-amygdala rsFC could predict four-week treatment response. Our results suggest that acupuncture may simultaneously modulate the rsFC of key regions in the descending pain modulation (PAG) and reward systems (VTA), and the amygdala may be a key node linking the two systems to produce antinociceptive effects. Our findings highlight the potential of acupuncture for chronic low back pain management. [ABSTRACT FROM AUTHOR]