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BACKGROUND AND HYPOTHESIS: Psychiatric comorbidities suggest that symptoms overlap across different diagnoses; the transdiagnostic network approach is valuable for studying psychopathology. Childhood trauma is a common transdiagnostic risk factor for psychiatric disorders, but the complex relationship between childhood trauma and psychopathology has seldom been investigated using a large cross-sectional transdiagnostic sample. STUDY DESIGN: This study recruited 869 patients with different diagnoses, including 418 schizophrenia, 215 bipolar disorder, and 236 major depressive disorder. Participants completed psychiatric interviews and self-report questionnaires. We constructed dimension- and item-level Least Absolute Shrinkage and Selection Operator-based (LASSO) networks to explore the relationship between childhood trauma, psychopathology, and duration of illness. Moreover, we constructed directed acyclic graphs (DAGs) to tentatively clarify the potential directions of associations among these variables. Network Comparison Tests (NCTs) were conducted for different diagnostic groups and gender-stratified groups. STUDY RESULTS: The transdiagnostic LASSO networks showed that different types of childhood trauma exerted distinct impacts on various psychopathological dimensions. Emotional abuse was linked to depressive symptoms, physical abuse to excited symptoms, sexual abuse to positive and disorganized symptoms, emotional neglect to depressive symptoms and motivation and pleasure (MAP) deficits factor of negative symptoms, and physical neglect to MAP factor. The DAG findings generally concurred with the LASSO network. The NCT showed comparable networks. CONCLUSIONS: Our findings suggest that childhood trauma is significantly associated with the development of psychopathology across different diagnostic groups. The affective pathway model suggests that early identification and tailored interventions would be needed for people with a history of childhood trauma.

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Theory of mind (ToM) and empathy are considered key components of social cognition that are often impaired in individuals with autism spectrum disorders (ASD). However, it remains unclear whether individuals with high levels of autistic traits exhibit similar impairments in these two functions. This study examined the affective and cognitive domains of ToM and empathy in individuals with high levels of autistic traits. We recruited 84 participants with high levels and 78 participants with low levels of autistic traits to complete a set of self-reported checklists and performance-based tasks capturing affective and cognitive components of ToM and empathy. The results showed that participants with high levels of autistic traits exhibited significant impairments in cognitive but not in affective ToM and empathy compared with their counterparts with low levels of autistic traits. We also found that empathy impairments in people with high levels of autistic traits were confounded by alexithymia and depressive traits.

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This study applied two incentive delay tasks involving social and non-social incentive types to 76 pairs of participants with high and low depressive symptoms. The results suggest that higher levels of depressive symptoms are correlated with abnormalities in social and non-social reward processing even in the healthy populations.

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Anhedonia and amotivation are core symptoms of schizophrenia (SCZ) and major depressive disorder (MDD). Reward processing involves constructing and contrasting the representations for expected value (EV) and outcome value (OV) of a given stimulus, a phenomenon termed range adaptation. Impaired range adaptation can lead to anhedonia and amotivation. This study aimed to examine range adaptation in SCZ patients and MDD patients. Fifty SCZ, 46 MDD patients and 56 controls completed the Effort-based Pleasure Experience Task to measure EV and OV adaptation. SCZ and MDD patients showed altered range adaptation, albeit in different patterns. SCZ patients exhibited over-adaptation to OV and reduced adaptation to EV. By contrast, MDD patients exhibited diminished OV adaptation but intact EV adaptation. Both OV and EV adaptation were correlated with anhedonia and amotivation in SCZ and MDD. Taken together, our findings suggest that range adaptation is altered in both SCZ and MDD patients. Associations of OV and EV adaptation with anhedonia and amotivation were consistently found in SCZ and MDD patients. Impaired range adaptation in SCZ and MDD patients may be putative neural mechanisms and potential intervention targets for anhedonia and amotivation.

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Range adaptation refers to the representation of a stimulus value based on its relative position in the range of pre-experienced values. Altered range adaptation in value representation may be related to motivation and pleasure (MAP) deficit in schizophrenia (SCZ). This follow-up study examined the relationship between range adaptation performance and MAP symptoms in SCZ patients. We recruited 26 schizophrenia patients and followed them for 1 year. They completed an experimental task for estimating their range adaptation to outcome value (OV) and expected value (EV) at baseline and after 1 year. At baseline, we found a marginally significant and negative correlation between OV adaptation and avolition symptoms in SCZ patients. Moreover, the 1-year change of EV adaptation was significantly and negatively correlated with the change of self-report pleasure experience. Our results suggest that range adaptation may track the variations of MAP symptoms in SCZ.

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Reward motivation in individuals with high levels of negative schizotypal traits (NS) has been found to be lower than that in their counterparts. But it is unclear that whether their reward motivation adaptively changes with external effort-reward ratio, and what resting-state functional connectivity (rsFC) is associated with this change. Thirty-five individuals with high levels of NS and 44 individuals with low levels of NS were recruited. A 3T resting-state functional brain scan and a novel reward motivation adaptation behavioural task were administrated in all participants. The behavioural task was manipulated with three conditions (effort > reward condition vs. effort < reward condition vs. effort = reward condition). Under each condition were rated 'wanting' and 'liking' for rewards. The seed-based voxel-wise rsFC analysis was conducted to explore the rsFCs associated with the 'wanting' and 'liking' ratings in individuals with high levels of NS. 'Wanting' and 'liking' ratings of individuals with high levels of NS significantly declined in the effort > reward condition but did not rebound as high as their counterparts in the effort < reward condition. The rsFCs in NS group associated with these ratings were altered. The altered rsFCs in NS group involved regions in the prefrontal lobe, dopaminergic brain regions (ventral tegmental area, substantia nigra), hippocampus, thalamus and cerebellum. Individuals with high levels of NS manifested their reward motivation adaptation impairment as a failure of adjustment adaptively during effort-reward imbalance condition and altered rsFCs in prefrontal, dopaminergic and other brain regions.

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Interoception, the sense of the physiological condition of our body, is impaired in individuals with autism spectrum disorders. Evidence suggests that subclinical autistic traits are mild manifestations of autistic symptoms, present in the general population. We examined the resting-state functional connectivity (rsFC) associating with interoception and autistic traits in 62 healthy young adults. Autistic traits correlated negatively with the rsFC between the lateral ventral anterior insula and anterior cingulate cortex. Interoceptive accuracy and sensibility correlated positively with the rsFC between interoceptive brain networks and the cerebellum, supplementary motor area, and visual regions. The results suggest that a negative relationship between interoception and autistic traits is largely accounted for by both self-report measures and decreased rsFC amongst the interoceptive brain network.

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This sequential mediation analysis study examined how the baseline effort-reward imbalance (ERI) would predict reward motivation 1 year later in 435 college students. We found that negative/disorganized schizotypal traits and anticipatory pleasure experience together mediate the prediction of ERI for reward motivation.

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OBJECTIVES: Childhood trauma (CT) has been found to increase the risk of developing schizophrenia and other psychiatric disorders. Little is known regarding the complex interplay between CT, subclinical psychotic, and affective symptoms in the general population. This cross-sectional study adopted network analysis to examine such a complex relationship. We hypothesized that CT would show strong connections with schizotypy dimensions, and the high schizotypy subgroup would show a network with higher global strength compared with the low schizotypy subgroup. METHODS: A total of 1813 college students completed a set of self-report questionnaires measuring CT, schizotypal features, bipolar traits, and depressive symptoms. The subscales of these questionnaires were used as nodes, and the partial correlations between nodes were used as edges to construct a network. Network Comparison Tests were used to investigate the differences between participants with high schizotypy and low schizotypy. An independent sample (n = 427) was used to examine the replicability of the results. RESULTS: Findings from the main dataset showed that CT was closely connected with schizotypy and motivation, after controlling for the inter-relationships between all nodes in the network. Relative to the low schizotypy subgroup, the network of the high schizotypy subgroup showed higher global strength. The two subgroups did not differ in network structure. Network analysis using the replication dataset showed comparable global strength and network structure. CONCLUSIONS: Our findings support specific links between CT and schizotypy dimensions in healthy youth populations, and such links appear to become stronger in those with high schizotypy.

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Major depressive disorder (MDD) is associated with deficits in emotion experience, expression and regulation. Whilst emotion regulation deficits prolong MDD, emotion expression influences symptomatic presentations, and anticipatory pleasure deficits predict recurrence risk. Profiling MDD patients from an emotion componential perspective can characterize subtypes with different clinical and functional outcomes. This study aimed to investigate emotional subtypes of MDD. A two-stage cluster analysis applied to 150 MDD patients. Clustering variables included emotion experience measured by Temporal Experience of Pleasure Scale, emotion expression measured by Toronto Alexithymia Scale, and emotion regulation measured by Emotion Regulation Questionnaire. We validated the resultant clusters by comparing their symptoms and functioning with that of 50 controls. Cluster 1 (n = 50) exhibited intact emotion experience and expression yet adopted reappraisal rather than suppression strategy, whereas Cluster 2 (n = 66) exhibited generalized emotional deficits. Cluster 3 (n = 34) exhibited emotion expression deficits and adopted both reappraisal and suppression strategies. On validation, Cluster 2 exhibited the worst, but Cluster 1 exhibited the least symptoms and social functioning impairments. Cluster 3 was intermediate among the two other subtypes. Our findings support the existence of different emotional subtypes in MDD patients, and have clinical and theoretical implications for developing future specific treatments for MDD.

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The schizotypy construct is useful for studying the effects of environmental stress on development of subclinical negative symptoms. The relationship among self-report motivation, effort-reward imbalance (ERI), and schizotypal features has seldom been studied. We aimed to examine the possible moderation effect of schizotypal traits on ERI and reward motivation. Eight-hundred-and-forty-three college students were recruited online to complete a set of self-reported measures capturing schizotypal traits, effort-reward imbalance and reward motivation, namely the Schizotypal Personality Questionnaire (SPQ), the Effort-Reward Imbalance-School Version Questionnaire (C-ERI-S) and the Motivation and Pleasure Scale-Self Report (MAP-SR). We conducted multiple linear regression to construct models to investigate the moderating effects of schizotypal traits on the relationship between ERI and reward motivation. Stressful ERI situation predicted the reduction of reward motivation. Negative schizotypal traits showed a significant negative moderating effect on the relationship between ERI and reward motivation, while positive and disorganized schizotypal traits had significant positive moderating effects. Schizotypal traits subtypes differently moderate the relationship between ERI and reward motivation. Only negative schizotypal traits and stressful ERI situation together have negative impact on reward motivation.

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Emotion processing and beliefs about pleasure can influence the development and severity of depressive symptoms. This cluster analysis study aimed to profile a large sample of college students using pleasure experience, emotion expression and regulation as well as beliefs about pleasure. We also aimed to validate the resultant clusters in terms of depressive symptoms. A set of checklists capturing beliefs about pleasure and the three facets of emotion processing was administered to 1028 college students. A two-stage cluster analysis was used to analyze the profile of these emotional aspects in these college students. Our results showed that a three-cluster solution best fit the data. Cluster 1 (n = 536) was characterized by moderate levels of beliefs about pleasure, pleasure experience, emotion expression, and regulation; Cluster 2 (n = 402) was characterized by generally high levels of beliefs about pleasure, pleasure experience, emotion expression, and regulation; Cluster 3 (n = 90) was characterized by relatively low levels of beliefs about pleasure, pleasure experience, emotion expression, and regulation. The three clusters differed significantly in the severity of depressive symptoms. Our findings suggest the existence of three emotional subtypes, which may be useful in early detection of youth at risk of developing depression.

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Altered social reward anticipation could be found in schizophrenia (SCZ) patients and individuals with high levels of social anhedonia (SA). However, few research investigated the putative neural processing for altered social reward anticipation in these populations on the SCZ spectrum. This study aimed to examine the underlying neural mechanisms of social reward anticipation in these populations. Twenty-three SCZ patients and 17 healthy controls (HC), 37 SA individuals and 50 respective HCs completed the Social Incentive Delay (SID) imaging task while they were undertaking MRI brain scans. We used the group contrast to examine the alterations of BOLD activation and functional connectivity (FC, psychophysiological interactions analysis). We then characterized the beta-series social brain network (SBN) based on the meta-analysis results from NeuroSynth and examined their prediction effects on real-life social network (SN) characteristics using the partial least squared regression analysis. The results showed that SCZ patients exhibited hypo-activation of the left medial frontal gyrus and the negative FCs with the left parietal regions, while individuals with SA showed the hyper-activation of the left middle frontal gyrus when anticipating social reward. For the beta-series SBNs, SCZ patients had strengthened cerebellum-temporal FCs, while SA individuals had strengthened left frontal regions FCs. However, such FCs of the SBN failed to predict the real-life SN characteristics. These preliminary findings suggested that SCZ patients and SA individuals appear to exhibit altered neural processing for social reward anticipation, and such neural activities showed a weakened association with real-life SN characteristics.

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The anterior insula (AI) has the central role in coordinating attention and integrating information from multiple sensory modalities. AI dysfunction may contribute to both sensory and social impairments in autism spectrum disorder (ASD). Little is known regarding the brain mechanisms that guide multisensory integration, and how such neural activity might be affected by autistic-like symptoms in the general population. In this study, 72 healthy young adults performed an audiovisual speech synchrony judgment (SJ) task during fMRI scanning. We aimed to investigate the SJ-related brain activations and connectivity, with a focus on the AI. Compared with synchronous speech, asynchrony perception triggered stronger activations in the bilateral AI, and other frontal-cingulate-parietal regions. In contrast, synchronous perception resulted in greater involvement of the primary auditory and visual areas, indicating multisensory validation and fusion. Moreover, the AI demonstrated a stronger connection with the anterior cingulate gyrus (ACC) in the audiovisual asynchronous (vs. synchronous) condition. To facilitate asynchrony detection, the AI may integrate auditory and visual speech stimuli, and generate a control signal to the ACC that further supports conflict-resolving and response selection. Correlation analysis, however, suggested that audiovisual synchrony perception and its related AI activation and connectivity did not significantly vary with different levels of autistic traits. These findings provide novel evidence for the neural mechanisms underlying multisensory temporal processing in healthy people. Future research should examine whether such findings would be extended to ASD patients.

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BACKGROUND: Negative symptoms are core symptom of schizophrenia, and many previous research studied the latent structure of negative symptoms based on a single measurement scale. Applying two second-generation negative symptom scales to the same sample can address measurement-invariance of latent structure. METHODS: Three-hundred-and-five schizophrenia patients were assessed using the CAINS and the BNSS. Confirmatory Factor Analysis (CFA) tested four competing factor-models: (1) a 1-factor model; (2) a 2-factor model comprising the motivation and pleasure (MAP) domain and the diminished expression (EXP) domain; (3) a 5-factor model comprising anhedonia, avolition, asociality, blunted affect and alogia; (4) a hierarchical model comprising the "first-order" 5-domain factors and the "second-order" MAP & EXP factors. RESULTS: The CFA results for the data of the CAINS showed that the 2-factor model had the best data fit over the other competing models. The CFA using the BNSS data in the same sample also supported the superiority of the 2-factor model. Lastly, after combining the items of the BNSS and CAINS together in the same sample for CFA, the 2-factor model prevailed over the other competing models. CONCLUSIONS: The 2-factor model appears to be measurement-invariant latent structure of negative symptoms. The novel method of combining the items of the CAINS and BNSS might have circumvented the possible imperfect construct of a single scale. Our findings support the MAP and EXP factors as the latent structure for negative symptoms.

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Altered hub regions in brain network have been consistently reported in patients with schizophrenia. However, it is unclear whether similar altered hub regions of the brain would be exhibited in individuals with subclinical features of schizophrenia such as social anhedonia (SA). In this study, we examined the hub regions of resting-state social brain network (SBN) of 35 participants with SA and 50 healthy controls (HC). We further examined the prediction effect of hub-connected FCs with SBN on the real-life social network characteristics. Our findings showed that the right amygdala, left temporal lobe and right media superior frontal gyrus were the hub regions of SBN both in SA and HC groups. In the SA group, the left temporal lobe connected functional connectivity (FC) did not predict social network characteristics, while the other FCs strengthened the association with social network characteristics. These findings were replicated in an independent sample of 33 SA and 32 HC. These findings suggested that the left temporal lobe as one of the hub regions of SBN exhibited the abnormality of their connected FCs in the association with social network characteristics in individuals with SA.

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Negative symptoms, particularly the motivation and pleasure (MAP) deficits, are associated with impaired social functioning in patients with schizophrenia (SCZ). However, previous studies seldom examined the role of the MAP on social functioning while accounting for the complex interplay between other psychopathology. This network analysis study examined the network structure and interrelationship between negative symptoms (at the "symptom-dimension" and "symptom-item" levels), other psychopathology and social functioning in a sample of 269 patients with SCZ. The psychopathological symptoms were assessed using the Clinical Assessment Interview for Negative Symptoms (CAINS) and the Positive and Negative Syndrome Scale (PANSS). Social functioning was evaluated using the Social and Occupational Functioning Assessment Scale (SOFAS). Centrality indices and relative importance of each node were estimated. The network structures between male and female participants were compared. Our resultant networks at both the "symptom-dimension" and the "symptom-item" levels suggested that the MAP factor/its individual items were closely related to social functioning in SCZ patients, after controlling for the complex interplay between other nodes. Relative importance analysis showed that MAP factor accounted for the largest proportion of variance of social functioning. This study is among the few which used network analysis and the CAINS to examine the interrelationship between negative symptoms and social functioning. Our findings supported the pivotal role of the MAP factor to determine SCZ patients' social functioning, and as a potential intervention target for improving functional outcomes of SCZ.

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Rhamnazin (RN) is a flavonol isolated from the calyxes and fruits of Physalis alkekengi L. var. franchetii (Mast.) Makino, which has been used for treating pulmonary diseases in traditional Chinese medicine. The nuclear factor erythroid 2-related factor 2 (Nrf2) is a therapeutic target for pulmonary diseases. In the present study, the underlying mechanism and pharmacological effect of RN against pulmonary disorders are investigated. Human lung epithelial Beas-2B cell and RAW 264.7 murine macrophage-based cell models, and a cigarette smoke (CS)-induced pulmonary impairment mice model are adopted for investigation in vitro and in vivo. RN is identified to be an Nrf2 activator, which promotes Nrf2 dissociation from Keap1 via reacting with the Cys151 cysteine residue of Keap1, and suppresses Nrf2 ubiquitination. In addition, RN is able to attenuate toxicant-stimulated oxidative stress and inflammatory response in vitro. Importantly, RN significantly relieves CS-induced oxidative insult and inflammation, and RN-induced inhibition of inflammation is related to inhibition of nuclear transcription factor-κB (NF-κB) and induction of cell autophagy. In conclusion, our data indicate that RN is an activator of the Nrf2 pathway and evidently alleviates pulmonary disorders via restricting NF-κB activation and promoting autophagy. RN is a promising candidate for the therapy of pulmonary disorders.

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The prevalence of obsessive-compulsive symptoms (OCS) in schizophrenia patients is as around 30%. Evidence suggested that mild OCS could reduce symptoms of schizophrenia, supporting the presence of compensatory functions. However, severe OCS could aggravate various impairments in schizophrenia patients, supporting the "double jeopardy hypothesis". Patients with schizo-obsessive comorbidity, schizophrenia patients and obsessive-compulsive disorder patients have been found to have similarities in executive dysfunctions and altered resting-state functional connectivity within the executive control network (ECN). Executive functions could be associated with the ECN. However, little is known as to whether such overlap exists in the subclinical populations of individuals with schizo-obsessive traits (SOT), schizotypal individuals and individuals with high levels of obsessive-compulsive symptoms (OCS). In this study, we recruited 30 schizotypal individuals, 25 individuals with OCS, 29 individuals with SOT and 29 controls for a resting-state ECN-related functional connectivity (rsFC) and a go/shift/no-go task. We found that individuals with SOT exhibited increased rsFC within the ECN compared with controls, while schizotypal individuals exhibited the opposite. Individuals with OCS exhibited decreased rsFC within the ECN and between the ECN and the default mode network (DMN), relative to controls. No significant correlational results between altered rsFC related to the ECN with executive function performance were found after corrections for multiple comparisons in three subclinical groups. Our findings showed that individuals with SOT had increased rsFC within the ECN, while schizotypal individuals and individuals with OCS showed the opposite. Our findings provide evidence for possible neural substrates of subclinical comorbidity of OCS and schizotypy.

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