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Despite consistent reports of the association between problematic internet gaming (PIG) and non-suicidal self-injury (NSSI), an increase in PIG does not necessarily lead to increased NSSI. This apparent paradox indicates the presence of other mediators and moderators in the PIG-NSSI association. This study aimed to investigate the role of anxiety as a potential moderating and mediating factor of the PIG-NSSI association in Chinese adolescents. A cross-sectional study was conducted among 10,479 Chinese adolescents (50.5% male; age range, 9–18 years). Standardized self-report questionnaires were used to assess the severity of PIG, anxiety, and NSSI. Spearman correlation and multiple linear regression were applied to examine the relationships among PIG, anxiety, and NSSI. Both moderating and mediating effects of anxiety were assessed using Hayes' methods. PIG, anxiety symptoms, and NSSI significantly correlated with one another. Anxiety significantly moderated the relationship between PIG and NSSI [B = 0.002, standard error (SE) = 0.000, p < 0.001], and it partially mediated the PIG-NSSI association [B = 0.017, SE = 0.001, 95% confidence interval (CI) 0.014–0.021]. Social concern and concentration were the two dimensions of anxiety that exerted the strongest mediation effect (B = 0.017, SE = 0.002, 95% CI 0.014–0.020). Adolescents with PIG and high anxiety are likely to suffer more severe NSSI and may benefit from interventions to reduce anxiety symptoms. •Chinese adolescents with problematic internet gaming (PIG) are more likely to engage in non-suicidal self-injury (NSSI).•Anxiety significantly moderates the PIG-NSSI association.•Anxiety partially mediates the PIG-NSSI association.

Background Mood disorder, impulsivity and aggression are common in drug users compared to healthy controls. However, no study has focused on the difference in various types of drug users. Therefore, the objective of this study was to explore the differences in depression, anxiety, impulsivity, and aggression among methamphetamine, heroin and polysubstance users and to further explore the risk factors for severe depression in the three groups. Methods Drug users over 18 years old who met the DSM-V diagnostic criteria for substance -related disorders were included in the study. All participants completed a general questionnaire, the Zung Self-Rating Depression Scale (SDS), the Zung Self-Rating Anxiety Scale (SAS), Barratt impulsiveness Scale Version 11 (BIS-11), and the Buss-Perry Aggression Questionnaire (BPAQ). One-way ANOVAs or Chi-square tests were used to test the differences among the groups, correlation analysis was used to test the relationship between drug use and other parameters, and multiple logistic regression was conducted to assess the risk factors for severe depression. Results A total of 1,486 participants were included, comprising 86.3% males with a mean age of 38.97 years. There was a significant difference in the percentage of severe depression and SDS scores among the three groups, but no significant difference was found in SAS, BIS-11 and BPAQ scores. Using methamphetamines, hostility and anxiety were risk factors for developing severe depression in all the participants and anxiety remained constant in the other three groups. Moreover, methamphetamine use was 2.16 and 3.35 times more likely to cause severe depression than heroin and polysubstance use, respectively. The initial age of substance use was negatively correlated with BPAQ, SAS, and SDS scores, whereas the drug use duration and addiction duration were positively correlated. Conclusions In this study, we found that the highest prevalence of severe depression was in participants using methamphetamines and that using methamphetamines, hostility, and anxiety were risk factors for developing severe depression. This result addressed an important gap in our knowledge of the different characteristics of depression, anxiety, impulsivity and aggression in various types of substance users and provides clinicians and policy-makers with directions for intervention and preventing relapse.

Background Methamphetamine (METH)-induced psychosis (MAP), characterized by transient schizophreniform symptoms, affects approximately 43% of individuals with methamphetamine use disorders (MUD). However, the cortical atrophy pattern associated with MAP remain unclear. Methods Ninety-four male patients with MUD (62 without psychotic symptoms [MA] and 32 MAP) and 61 healthy controls (HCs) underwent high-resolution T1-weighted MRI and clinical assessments. Surface-based morphological (SBM) analysis using FreeSurfer 7.1.1 was conducted to explore cortical thickness and volume difference among groups. We also examined the correlation between brain structural changes and clinical variables. Results The MAP group showed significant cortical thinning in the left superior temporal gyrus (STG) and the right rostral anterior cingulate cortex (rACC) whether compared to HCs and MA. Additionally, compared to the HCs, the MA group exhibited decreased cortical volume in the left caudal middle frontal gyrus (cMFG) and the superior parietal cortex (SPC). In the MUD cohort, left cMFG volume was positively correlated with craving severity (VAS score, r  = 0.341, p  < 0.001). Conclusions MAP is associated with distinct region-specific cortical thinning, particularly in temporal and limbic regions, suggesting a structural basis for its psychotic features. These findings provide new insight into the neurobiological mechanisms underlying MAP and may inform future intervention strategies. Clinical trial number Not applicable.

Background Sustained attention deficits were reported more significant in patients with major depressive disorder (MDD) than in healthy controls (HCs), and are pivotal in both the development and aggravation of depression. Childhood trauma is also common in MDD and the exposure to childhood trauma may impede sustained attention and increase the treatment resistance in MDD. However, the underlying neuro-mechanisms link the childhood trauma to sustained attention deficits in MDD remain unclear. Methods We collected resting-state functional magnetic resonance imaging data, and measured childhood trauma severity using the Childhood Trauma Questionnaire and sustained attention using the Continuous Performance Test, Identical Pairs version. After excluding subjects with significant head movement, 45 MDDs and 54 HCs were included in the analysis. We compared fractional amplitude of low-frequency fluctuation (fALFF) between the groups, conducted whole-brain correlation analysis between the fALFF and sustained attention in the MDD group, and defined significant regions as the regions of interest for the seed-to-whole brain functional connectivity (FC) analysis. We further performed mediation analyses to investigate the relationships among the childhood trauma, fALFF and FC values, and the level of sustained attention in the MDD group. Results Compared with HCs, MDDs exhibited higher fALFF in the right middle frontal gyrus and left inferior frontal gyrus, and lower fALFF in the bilateral insular cortex, left medial orbital superior frontal gyrus and left angular gyrus (ANG.L). Whole-brain correlation analysis showed that impaired sustained attention was associated with increased fALFF in the left postcentral gyrus (PoCG.L), and FC of PoCG.L-left precentral gyrus (PreCG.L) and ANG.L-right superior temporal gyrus (STG.R) in the MDD group. Furthermore, mediation analyses showed that the fALFF in PoCG.L, and FC of PoCG.L-PreCG.L and ANG.L-STG.R mediated the relationship between the childhood trauma and sustained attention in the MDD group. Conclusion The fALFF in PoCG.L, and FC of PoCG.L-PreCG.L and ANG.L-STG.R might be potential neural substrate in the association between the childhood trauma and poor sustained attention in the MDDs, and might serve as potential intervention targets for the treatment of sustained attention deficits in MDDs with childhood trauma history.

Background Tourette syndrome (TS) is a neuropsychiatric disorder characterized by repetitive and patterned tics. Its onset correlates with dysfunctions in immunological activation and neurotransmitters. Autoimmune movement disorders such as dopamine-2 receptor antibody encephalitis (D2R encephalitis) may go undiagnosed in TS patients seeking medical help for tic symptoms only. Here, we present a clinical case of D2R encephalitis in a TS patient. Case presentation A 13-year-old boy with a history of TS presented with acute tongue-biting without positive neurologic examination or auxiliary examination results, except for a weakly positive finding for D2R antibodies in the serum sample. He was initially diagnosed with possible D2R encephalitis, but the influence of TS could not be ruled out. In addition to psychotropics, we administered immunotherapy early based on clinical characteristics, and his symptoms were ameliorated significantly. During the follow-up, he was diagnosed with definite D2R encephalitis, and the dosage of psychotropics was further adjusted for fluctuating symptoms. Conclusions Our case suggests that clinicians should discern D2R encephalitis in TS patients when tics are the primary symptoms. Administering immunotherapy early, according to clinical characteristics, may benefit the patient. Moreover, the features of premonitory urges could help evaluate the state of TS.

Methamphetamine use disorder (MUD) represents a substantial global health challenge, largely attributable to the absence of effective treatments stemming from limited understanding of its neurobiological mechanisms. This study aimed to investigate the structural brain alterations, trait impulsivity, and genetic factors underlying MUD. We conducted structural magnetic resonance imaging scanning and whole-exome sequencing on a cohort of 142 male participants (91 patients with MUD vs. 51 healthy controls). Voxel-based morphometry revealed a significant reduction in gray matter volume (GMV) in the left thalamus among MUD patients, which exhibited a negative correlation with motor impulsivity (MI). Mediation analysis further demonstrated that MI mediated the relationships between thalamic GMV, duration of drug use, and MUD severity. Gene- and gene set-based burden tests identified 72 genes and three biological pathways: Cytidine Analogs Cytotoxicity, Muscle Structure Development, and Nuclear Speck, that were significantly associated with thalamic volume. GO enrichment analyses of 362 common genetic variants indicated a significant involvement in ciliary and microtubule-based motility processes. Concurrently, KEGG pathway analyses highlighted cytoskeletal and extracellular matrix signaling pathways. Gene-environment interaction analyses revealed that thalamic volume was significantly influenced by the interaction between rs12729569 and METH use, as well as between rs2282440 and duration of use. These findings suggest the thalamus as a critical structural substrate that links impulse control with METH-related neurotoxicity, emphasizing the role of cytoskeletal dynamics and ciliary function. Genetic variants that influence thalamic vulnerability may serve as promising biomarkers for risk stratification and the development of personalized interventions in MUD.

IntroductionThe cognitive dysfunction associated with nitrous oxide abuse is gradually becoming a major global public health concern. Despite the increasing prevalence of nitrous oxide abuse, there are currently no authorised/approved treatment options. Hyperbaric oxygen therapy (HBOT) has been proven to be an efficient method to improve cognitive function. The current randomised, double-blinded, placebo-controlled trial will explore the effect of HBOT on cognitive dysfunction induced by nitrous oxide abuse.Methods and analysisEighty participants who abuse nitrous oxide and have cognitive dysfunction, including memory decline, disorientation, attention deficits, slower reactions and learning disabilities, will be included in the trial. They will be randomly assigned to receive either HBOT or sham-HBOT 90–120 min once daily for 5 days per week for 2 weeks. The primary outcome will be the improvement in the total score of the MATRICS Consensus Cognitive Battery, which will measure comprehensive cognitive function between the two groups. Additionally, attention will be measured by integrated visual and auditory continuous performance tests, executive function will be measured by the Wisconsin card sorting test, intelligence will be measured by Raven’s standard progressive matrices and cognitive control will be measured by the Stroop colour word interference test.Ethics and disseminationThis protocol was approved by the West China Hospital of Sichuan University Biomedical Research Ethics Committee. The report of the study will be disseminated via scientific forums including peer-reviewed publications and presentations at national and international conferences.Trial registration numberChinese Clinical Trial Registry (ChiCTR2100047111).

Methamphetamine (METH) dependence is a globally significant public health concern with no efficacious treatment. Trait impulsivity is associated with the initiation, maintenance, and recurrence of substance abuse. However, the presence of these associations in METH addiction, as well as the underlying neurobiological mechanisms, remains incompletely understood. We scanned 110 individuals with METH use disorder (MUDs) and 55 matched healthy controls (HCs) using T1-weighted imaging and assessed their drug use characteristics and trait impulsivity. Surface-based morphometry and graph theoretical analysis were used to investigate group differences in brain morphometry and network attributes. Partial correlations were conducted to investigate the relationships between brain morphometric changes, drug use parameters, and trait impulsivity. Mediation analyses examined how trait impulsivity and drug craving influenced the link between brain morphometric change and MUD severity in patients. MUDs exhibited thinner thickness in the left fusiform gyrus and right pars opercularis, as well as diminished small-world properties in their structural covariance networks (SCNs) compared to HCs. Furthermore, reduced cortical thickness in the right pars opercularis was linked to motor impulsivity (MI) and MUD severity, and the association between the right pars opercularis thickness and MUD severity was significantly mediated by both MI and cue-induced craving. These findings suggest that MUDs exhibit distinct brain structural abnormalities in both the cortical thickness and SCNs and highlight the critical role of impulse control in METH addiction. This insight may offer a potential neurobiological target for developing therapeutic interventions to treat addiction and prevent relapse.

Background The high prevalence of nonsuicidal self-injury (NSSI) in youths demonstrates a substantial population-level burden on society. NSSI is often associated with emotional and social skill deficits. To date, several studies have aimed to identify the underlying neural mechanism of those deficits in NSSI by using functional magnetic resonance imaging (fMRI). However, their conclusions display poor consistency. Objective We aimed to conduct a meta-analysis using activation likelihood estimation (ALE) for fMRI data based on emotional and cognitive tasks to clarify the underlying neural processing deficits of NSSI. Methods We searched for MRI studies of NSSI in the PubMed, Cochrane, and Embase databases. We identified significant foci for the included studies and conducted two ALE meta-analyses as follows: (i) activation for the NSSI contrast healthy control group and (ii) deactivation for the NSSI contrast healthy controls. Considering the diverse sex composition of study participants and possible bias from one large sample study, we conducted sensitivity analyses for the meta-analysis. Results Nine studies comprising 359 participants were included, and the results demonstrated substantial activation in NSSI patients compared with healthy controls in two clusters located in the right medial frontal gyrus extending to the rostral anterior cingulate and the left inferior frontal gyrus extending to the insula. Conclusions The results suggest that individuals with NSSI show brain activity alterations that underpin their core symptoms, including poor emotional regulation and reward processing deficits. Our findings provide new insights into the neural mechanism of NSSI, which may serve as functional biomarkers for developing effective diagnosis and therapeutic interventions for these patients.

Background The ε4 allele of apolipoprotein E gene ( APOE ) stands as the greatest genetic risk factor for late-onset Alzheimer’s disease (AD). Although microglia accumulating lipid droplets (LDAM) have been implicated in AD pathogenesis, the mechanistic link between ApoE4 and microglial lipid dysregulation remains elusive. Methods We employed a multi-omics approach, combining snRNA-seq and locus-specific epigenetic analysis, alongside microglia-specific gene manipulation in ApoE-targeted replacement (TR) mice. Primary microglia were challenged with cholesterol to simulate lipid overload conditions. Results In mid-life ApoE4-TR mice, microglia within the dentate gyrus developed pronounced lipid droplet accumulation, concurrent with impaired Aβ clearance and a pro-inflammatory shift. snRNA-seq unveiled a unique microglial cluster in ApoE4 mice, enriched for lipid-metabolism genes and marked by the pronounced downregulation of the hub gene Asxl1. Mechanistically, ApoE4 attenuated the Asxl1–LXRα interaction, leading to reduced H3K4me3 occupancy at promoters of lipid-efflux genes such as Abca1. Crucially, CRISPR-mediated, microglia-specific overexpression of Asxl1 restored H3K4me3 levels, normalized cholesterol efflux, and rescued Aβ phagocytic deficits in vivo. Conclusions Our findings define an epigenetic pathway whereby ApoE4 drives microglial dysfunction via the Asxl1–LXRα–H3K4me3 axis, fostering the LDAM phenotype. Enhancing Asxl1 function presents a promising therapeutic avenue for countering ApoE4-mediated pathogenesis in AD.