General Psychiatry最新文献

{"title":"Shared genetic variants across substance use disorders implicate common neurobiological pathways, a genome-wide mixed methods study.","authors":"Børge Holen, Zillur Rahman, Alexey A Shadrin, Romain Icick, Kevin S O'Connell, Linn Rødevand, Nadine Parker, Markos Tesfaye, Piotr Jaholkowski, Oleksandr Frei, Anders M Dale, Srdjan Djurovic, Ole A Andreassen, Olav B Smeland","doi":"10.1002/gps3.70017","DOIUrl":"https://doi.org/10.1002/gps3.70017","url":null,"abstract":"<p><strong>Background: </strong>Substance use disorders (SUDs) are highly heritable, but the extent of shared and distinct genetic architecture across different SUDs is unclear.</p><p><strong>Aims: </strong>To compare the genetic architectures of alcohol use disorder (AUD), cannabis use disorder (CUD) and opioid use disorder (OUD) and to identify shared and unique genetic loci.</p><p><strong>Methods: </strong>We analysed large-scale genome-wide association study (GWAS) summary statistics from individuals of European ancestry recruited in Europe and the USA. The mixture model MiXeR was used to estimate the unique genetic architecture characteristics of each SUD, including its polygenicity, single nucleotide polymorphism (SNP)-heritability and discoverability, a measure of the distribution of genetic signal across all causal variants. Pairwise conditional/conjunctional false discovery rate (cond/conjFDR) analyses identified shared loci, followed by biological annotation of implicated genes.</p><p><strong>Results: </strong>AUD demonstrated the highest polygenicity, followed by CUD and OUD. SNP-based heritability was 0.10 for AUD and OUD and 0.01 for CUD. Discoverability was highest for OUD, followed by AUD and CUD. Currently, genome-wide significant SNPs explain 2.0% of AUD, 0.3% of CUD and 0.2% of OUD variance. Cond/conjFDR identified 39 novel loci for AUD, 10 for CUD and 1 for OUD. Of implicated genes, most were expressed in the brain, including several involved in gamma-aminobutyric acid and dopaminergic neurotransmission, opioid neurophysiology, myelination, DNA recombination, apoptosis and ubiquitin-dependent protein catabolism.</p><p><strong>Conclusions: </strong>SUDs have polygenic architectures with many shared loci and are similar with regards to some characteristics. However, the level of polygenicity differs across SUDs, with AUD being considerably more polygenic than OUD, whereas CUD is intermediate in terms of its polygenicity. The novel loci implicate genes primarily expressed in the brain, involving a variety of biological functions. The findings expand our view of the aetiology of these disorders, while supporting the hypothesis of a shared set of pleiotropic SUD genes.</p>","PeriodicalId":12549,"journal":{"name":"General Psychiatry","volume":"39 2","pages":"e70017"},"PeriodicalIF":6.8,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13095382/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147768816","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correspondence between morphological similarity of the left lateral orbitofrontal cortex and neurotransmitter systems in adolescent males with autism.","authors":"Huashuang Zhang, Junle Li, Chensheng Hou, Yilin Huang, Lisha Ma, Bincan Xiong, Jinhui Wang, Xuchu Weng","doi":"10.1002/gps3.70014","DOIUrl":"10.1002/gps3.70014","url":null,"abstract":"<p><strong>Background: </strong>Autism spectrum disorder (ASD) is a neurodevelopmental condition marked by pronounced heterogeneity in brain structure, which limits the development of targeted interventions. Morphological brain networks (MBNs) enable the mapping of coordinated structural features across brain regions at the individual level. However, the specific organisation of such networks in ASD and their potential relationships with underlying neurotransmitter systems remain largely unexplored.</p><p><strong>Aims: </strong>To characterise alterations in cortical thickness-based MBNs among adolescent males with ASD and to test whether these network changes spatially correspond to normative positron emission tomography-derived neurotransmitter receptor/transporter maps.</p><p><strong>Methods: </strong>In this cross-sectional study, T1-weighted magnetic resonance imaging (MRI) data from 424 adolescent males (207 with ASD, 217 typically developing) in the Autism Brain Imaging Data Exchange were analysed. MBNs were constructed using interregional cortical thickness similarity quantified by Jensen-Shannon divergence. Graph theoretical metrics were computed, and group differences were assessed with permutation tests controlling for age and intelligence quotient (IQ). Spatial correlations between left lateral orbitofrontal morphological similarity and atlas-based neurotransmitter maps were investigated using the JuSpace toolbox.</p><p><strong>Results: </strong>The ASD group exhibited a significantly increased normalised clustering coefficient (<i>t</i> = 2.40, <i>p</i> = 0.020) and decreased nodal centrality in the left lateral orbitofrontal cortex (OFC). This region showed reduced morphological similarity with 65 other brain regions. Furthermore, the OFC-based similarity patterns were significantly associated with the spatial distributions of gamma-aminobutyric acid type A (GABAa), 5-hydroxytryptamine receptor 1A (5-HT1a) and μ-opioid receptor systems (<i>r</i> = 0.22, <i>p</i> = 0.017, spin-corrected). These alterations were robust to stringent cross-family correction.</p><p><strong>Conclusions: </strong>These findings highlight the left lateral OFC as a structural key hub in adolescent males with ASD. The robustness of these OFC-centred network alterations under stringent cross-family correction, together with their associations with neurotransmitter systems, provides a potential neurobiological basis for targeted interventions in this population.</p>","PeriodicalId":12549,"journal":{"name":"General Psychiatry","volume":"39 2","pages":"e70014"},"PeriodicalIF":6.8,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13090103/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147722461","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Olfactory enrichment mitigates delayed neurocognitive recovery after major orthopaedic surgery in older patients: A randomised controlled trial.","authors":"Xinchun Mei, Zihan Ni, Shiyu Zhong, Jiayi Wang, Lin Zhu, Zhongyong Shi, Yupeng Chen, Hailin Zheng, Jingxiao Hu, Yuan Shen","doi":"10.1002/gps3.70022","DOIUrl":"https://doi.org/10.1002/gps3.70022","url":null,"abstract":"<p><strong>Background: </strong>Delayed neurocognitive recovery (dNCR) is a prevalent complication in older patients undergoing surgery. It may progress to long-term cognitive impairment and increase the risk of Alzheimer's disease.</p><p><strong>Aims: </strong>This study aimed to evaluate the effects of olfactory enrichment on dNCR and to examine the association between olfactory function and dNCR.</p><p><strong>Methods: </strong>This sham-controlled, assessor-blind, parallel-group randomised trial enrolled 149 participants aged 65 or older undergoing elective total knee or hip replacement under general anaesthesia. Participants were assigned to either the olfactory enrichment group or the sham group. The intervention group received daily olfactory enrichment from 3 days preoperatively to 7 days postoperatively. Cognitive function was evaluated using a neuropsychological test battery 3 days before and 7 days after surgery. Olfactory identification ability was assessed by five-odour olfactory detection arrays. Propensity score matching analysis was employed to mitigate potential confounding and selection bias.</p><p><strong>Results: </strong>A total of 131 patients completed the study (62 in the olfactory enrichment group and 69 in the sham group). The overall incidence of dNCR was 26.7% (35 out of 131). In the intention-to-treat analysis, the difference between groups was not statistically significant (19.4% vs. 33.3%; <i>χ</i> ² = 3.259; <i>p</i> = 0.071). However, in the 1:1 propensity score-matched cohort (<i>n</i> = 82), the incidence of dNCR was significantly lower in the olfactory enrichment group than in the sham group (12.2% vs. 39.0%; <i>χ</i> ² = 7.476; <i>p</i> = 0.005). Raw postoperative cognitive scores and individual change scores did not differ between the groups. Participants with decreased olfactory identification scores (<i>n</i> = 32) had a significantly higher incidence of dNCR than those with stable or improved scores (40.6% vs. 22.2%; <i>χ</i> ² = 4.183; <i>p</i> = 0.041).</p><p><strong>Conclusions: </strong>In older patients undergoing major orthopaedic surgery, perioperative olfactory dysfunction is associated with an increased risk of dNCR. Olfactory enrichment may represent a potential nonpharmacological strategy for reducing postoperative cognitive decline in this population.</p>","PeriodicalId":12549,"journal":{"name":"General Psychiatry","volume":"39 ","pages":"e70022"},"PeriodicalIF":6.8,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13140845/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147836639","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Causal machine learning analysis identifies subpopulations most likely to benefit from healthy lifestyles for cognitive outcomes.","authors":"Youjin Jiang, Yi Ding, Qiuyu Cao, Xianglin Wu, Xiaoran Li, Yu Xu, Zhiyun Zhao, Min Xu, Jieli Lu, Tiange Wang, Guang Ning, Weiqing Wang, Yufang Bi, Yuchen Xu, Mian Li","doi":"10.1002/gps3.70013","DOIUrl":"https://doi.org/10.1002/gps3.70013","url":null,"abstract":"<p><strong>Background: </strong>With dementia posing an escalating public health threat, adopting healthy lifestyles is increasingly recognised as a key preventive measure for preserving cognitive function. However, the effect of multidomain lifestyle intervention on cognitive health remains inconclusive and likely heterogeneous.</p><p><strong>Aims: </strong>We aimed to investigate the heterogeneity in the associations between healthier lifestyles and cognitive outcomes (cognitive performance and incident dementia) across identifiable subpopulations and to use causal machine learning to identify participant characteristics predictive of greater benefit.</p><p><strong>Methods: </strong>Causal machine learning analyses were performed using two prospective cohorts. The English Longitudinal Study of Ageing (ELSA) (waves 4-9, 2008-2018) served as the discovery cohort and the Health and Retirement Study (HRS) (waves 9-14, 2008-2018) served as the validation cohort. Healthy lifestyles included smoking status, alcohol consumption, physical activity and social contact. Global cognitive <i>z</i>-scores were computed based on standardised tests of memory, executive function and orientation. Dementia diagnoses were ascertained by integrating physician evaluations with measures of cognitive and functional performance.</p><p><strong>Results: </strong>We analysed 8771 participants from ELSA and 8531 participants from HRS. High-benefit groups displayed substantially improved cognitive performance (ELSA: mean: 0.27, 95% confidence interval [CI] 0.24-0.30; HRS: mean: 0.51, 95% CI 0.48-0.54) and reduced risk of dementia (ELSA: hazard ratio [HR]: 0.28, 95% CI 0.21-0.34; HRS: HR: 0.22, 95% CI 0.17-0.27). Subgroups deriving greater benefits in cognitive performance were younger and had higher baseline cognitive reserve, superior physical and respiratory function, and better cardiometabolic profiles with particularly lower blood pressure. Those deriving greater benefits in incident dementia were likewise younger, with higher baseline cognition and superior vascular metrics, including lower blood pressure.</p><p><strong>Conclusions: </strong>The cognitive benefits of healthy lifestyles vary by individual characteristics, underscoring the potential of personalised prevention strategies. Future randomised clinical trials are warranted to validate these findings and refine intervention approaches.</p>","PeriodicalId":12549,"journal":{"name":"General Psychiatry","volume":"39 ","pages":"e70013"},"PeriodicalIF":6.8,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13099276/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147768767","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sevoflurane versus propofol and the long-term risk of attention-deficit/hyperactivity disorder in children.","authors":"Mingyang Sun, Yangyang Wang, Yuqin Tang, Peilin Xie, Tian Mao, Zhongyuan Lu, Jiao Wang, Liang Zhao, Saihao Fu, Mengrong Miao, Wan-Ming Chen, Szu-Yuan Wu, Jiaqiang Zhang","doi":"10.1002/gps3.70000","DOIUrl":"10.1002/gps3.70000","url":null,"abstract":"<p><strong>Background: </strong>Preclinical studies have shown that volatile anaesthetics, particularly sevoflurane, can disrupt neurodevelopment by inducing neuronal apoptosis, neuroinflammation and altered synaptic plasticity during critical periods of brain maturation. Whether these mechanisms translate into long-term neurobehavioral risk in children remains uncertain.</p><p><strong>Aims: </strong>To compare the long-term risk of attention-deficit/hyperactivity disorder (ADHD) following paediatric anaesthesia with sevoflurane versus propofol in a large, multinational real-world cohort.</p><p><strong>Methods: </strong>We conducted a large, multinational, retrospective cohort study using real-world electronic health record data from more than 150 healthcare organisations across North America, Europe and Asia. Children and adolescents (0-18 years) who underwent a single surgical procedure under general anaesthesia between 2005 and 2025 were included. Patients with ADHD or multiple anaesthetic exposures were excluded. The primary exposure was sevoflurane versus propofol as the main anaesthetic. The primary outcome was new-onset ADHD identified by International Classification of Diseases, Ninth or Tenth Revision codes after surgery. Propensity-score matching (1:1), subgroup, sensitivity and positive/negative control analyses were performed to ensure robustness.</p><p><strong>Results: </strong>Among 54 102 matched children (27 051 per group), the cumulative incidence of ADHD was 5.63% after sevoflurane and 2.95% after propofol, corresponding to incidence rates of 134.9 and 105.4 per 10 000 person-years. Sevoflurane exposure was associated with a higher risk of ADHD (hazard ratio 1.21; 95% confidence interval 1.11-1.31; <i>p</i> < 0.001). Findings were consistent across subgroups and sensitivity analyses; mortality was rare and similar between groups.</p><p><strong>Conclusions: </strong>In this multinational cohort, sevoflurane exposure during paediatric anaesthesia was associated with an increased long-term risk of ADHD compared with propofol. These findings suggest that anaesthetic choice may have enduring neurobehavioral consequences and that prospective validation is warranted to guide safer paediatric anaesthesia practice.</p>","PeriodicalId":12549,"journal":{"name":"General Psychiatry","volume":"39 2","pages":"e70000"},"PeriodicalIF":6.8,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13084326/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147722498","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Global burden, risk factors and projections of self-harm mortality in adults aged 65+ years: A 60-year trend analysis from the Global Burden of Disease Study 2021.","authors":"Jinjie Xu, Yiman Guo, Zizhao Feng, Meiti Wang, Chengwei Guo, Yuan Feng","doi":"10.1002/gps3.70019","DOIUrl":"https://doi.org/10.1002/gps3.70019","url":null,"abstract":"<p><strong>Background: </strong>Epidemiological research on self-harm in older adults (aged 65+ years) remains scarce despite its growing public health significance amid global ageing.</p><p><strong>Aims: </strong>This study aimed to analyse the global burden, risk factors and projections of self-harm mortality in adults aged 65+ years from 1990 to 2050.</p><p><strong>Methods: </strong>Utilising data from the Global Burden of Disease Study 2021, this research examined the spatiotemporal patterns of self-harm mortality and years of life lost by age, gender and socio-demographic index (SDI) in adults aged 65+ across 204 countries and territories (grouped into 21 regions) from 1990 to 2021. It also explored the changes during the coronavirus disease 2019 pandemic, identified key risk factors and projected the future burden of self-harm mortality through 2050.</p><p><strong>Results: </strong>Global self-harm deaths among older adults increased from 116 642 in 1990 to 167 920 in 2021, a rise of 43.96%. However, the age-standardised mortality rate (ASMR) decreased by 39.56%, from 36.83 to 22.26 per 100 000. In 2021, central sub-Saharan Africa had the highest ASMR at 61.35 per 100 000, while North Africa and the Middle East recorded the lowest at 4.88 per 100 000. Male ASMR was 2.5 times as high as that of females (33.61 vs. 13.58 per 100 000), and adults aged 85 years and older were at particularly elevated risk. High alcohol use was identified as a major risk factor, especially for males. A U-shaped relationship between ASMR and the SDI was observed, with the lowest point at an SDI of approximately 0.70. Projections indicate a further 46.05% decline in ASMR to 12.01 per 100 000 by 2050.</p><p><strong>Conclusions: </strong>These results highlight complex global trends in self-harm mortality and associated risk factors among older adults, emphasising the urgent need for sex-, age-, and region-specific interventions, enhanced social support and systematic risk monitoring to inform age-friendly self-harm prevention policies, and sustainable development support goals.</p>","PeriodicalId":12549,"journal":{"name":"General Psychiatry","volume":"39 ","pages":"e70019"},"PeriodicalIF":6.8,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13137939/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147836560","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dynamic trajectories of neuropsychiatric symptoms predict Alzheimer's disease risk and clinical phenotypes.","authors":"Wenzheng Liu, Yan Wang, Yuhang Shi, Liangyu Huang, Chenchen Tan, Lan Tan, Wei Xu","doi":"10.1002/gps3.70018","DOIUrl":"https://doi.org/10.1002/gps3.70018","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;Neuropsychiatric symptoms (NPS) may serve as early predictors of Alzheimer's disease (AD). However, NPS evolve over time, and most existing studies have relied on single or sparse assessments that do not capture clinically meaningful longitudinal patterns.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Aims: &lt;/strong&gt;To examine whether distinct trajectories of NPS are associated with the risk of incident AD, neurodegeneration and cognitive decline.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;NPS were assessed using the neuropsychiatric inventory questionnaire. We first characterised and compared the retrospective trajectories of NPS between 290 incident AD dementia cases and 74 healthy controls who remained free of dementia during 8 years of follow-up. Latent class growth modelling was then applied to identify NPS trajectories over the first 3 years among 982 people without dementia at baseline. Cox regression and linear mixed-effects models were used to investigate the associations between NPS trajectories and incident AD risk, cognitive decline, brain atrophy and changes in brain metabolism during early (baseline to year 3) and later (years 3-8) follow-up periods. Interaction between NPS trajectories and &lt;i&gt;APOE&lt;/i&gt; ε4 was examined. Causal mediation analyses were conducted to assess whether neurodegeneration mediated the associations between NPS trajectories and cognitive function.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;Compared to individuals who remained free of dementia, people who developed AD showed progressively increasing NPS levels prior to AD diagnosis (&lt;i&gt;p&lt;/i&gt; &lt; 0.005). Three NPS trajectories were identified: consistently no symptoms (71.8%, as reference), increasing trajectory (18.6%) and remitting trajectory (9.6%). The increasing trajectory was significantly associated with a higher risk of AD during both the early (hazard ratio [HR] = 1.720, &lt;i&gt;p&lt;/i&gt; &lt; 0.001) and late (HR = 2.130, &lt;i&gt;p&lt;/i&gt; = 0.026) follow-up periods. The remitting trajectory was associated with an elevated risk of AD only in the early follow-up (HR = 1.980, &lt;i&gt;p&lt;/i&gt; &lt; 0.001). The increasing trajectory was also linked to faster brain atrophy (&lt;i&gt;β&lt;/i&gt; = -139.662, &lt;i&gt;p&lt;/i&gt; &lt; 0.001 for the hippocampus, &lt;i&gt;β&lt;/i&gt; = -108.642, &lt;i&gt;p&lt;/i&gt; = 0.007 for the entorhinal cortex and &lt;i&gt;β&lt;/i&gt; = -305.059, &lt;i&gt;p&lt;/i&gt; = 0.003 for the middle temporal regions), greater declines in brain metabolism (&lt;i&gt;β&lt;/i&gt; = -0.013, &lt;i&gt;p&lt;/i&gt; = 0.007) and accelerated cognitive deterioration (&lt;i&gt;β&lt;/i&gt; = -0.162 for the memory, &lt;i&gt;β&lt;/i&gt; = -0.154 for the executive function, all &lt;i&gt;p&lt;/i&gt; &lt; 0.001) during the late follow-up period. These associations were stronger among &lt;i&gt;APOE&lt;/i&gt; ε4 carriers. Brain volume loss and metabolism decline partially mediated the relationships of increasing NPS and cognitive impairment.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusions: &lt;/strong&gt;NPS trajectories can predict AD risk, neurodegeneration and cognitive decline, especially among &lt;i&gt;APOE&lt;/i&gt; ε4 carriers. Progressive neurodegenerative changes may underlie these associ","PeriodicalId":12549,"journal":{"name":"General Psychiatry","volume":"39 ","pages":"e70018"},"PeriodicalIF":6.8,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13111414/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147768765","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Peer bullying victimisation and depressive symptoms as serial mediators between attention-deficit/hyperactivity disorder symptoms and internet gaming disorder among Chinese adolescents: A three-wave longitudinal study.","authors":"Pu Peng, Zhangming Chen, Silan Ren, Ying He, Jinguang Li, Aijun Liao, Linlin Zhao, Xu Shao, Shanshan Chen, Ruini He, Yudiao Liang, Youguo Tan, Xiaogang Chen, Jinsong Tang, Yanhui Liao","doi":"10.1002/gps3.70012","DOIUrl":"https://doi.org/10.1002/gps3.70012","url":null,"abstract":"<p><strong>Background: </strong>The association between attention-deficit/hyperactivity disorder (ADHD) symptoms and internet gaming disorder (IGD) is well-established, yet the psychological mechanisms underlying this comorbidity remain underexplored.</p><p><strong>Aims: </strong>Grounded in the dual failure model and the compensatory internet use model, this study examined peer bullying victimisation and depressive symptoms as serial mediators in the longitudinal association between ADHD symptoms and IGD severity among 20 137 Chinese adolescents.</p><p><strong>Methods: </strong>Participants were assessed at baseline (T1, November 2020) and followed up at one (T2) and two years (T3). Standardised measures assessed peer bullying victimisation (Multidimensional Peer Victimisation Scale), ADHD symptoms (Strengths and Difficulties Questionnaire), depressive symptoms (9-item Patient Health Questionnaire) and IGD severity (Internet Gaming Disorder Scale-Short Form). Longitudinal path analysis with serial mediation tested the hypothesised pathway, adjusting for baseline covariates and prior symptoms. Subgroup analyses examined sex and developmental (early vs. late adolescence) differences. Sensitivity analyses included alternative mediation models, cross-lagged panel models and parallel-process latent growth curve models.</p><p><strong>Results: </strong>Baseline ADHD symptoms directly predicted IGD severity and indirectly through peer bullying victimisation and depressive symptoms. These mediators accounted for one-third of the total effect. The bullying-related mediation pathway was evident only among boys and early adolescents, whereas depressive symptoms consistently mediated the association across sexes and age groups. Sensitivity analyses supported the robustness and temporal specificity of the proposed pathway.</p><p><strong>Conclusions: </strong>ADHD symptoms increase the risk of subsequent IGD through both direct and indirect pathways operating through peer bullying victimisation and depressive symptoms. This social-emotional mediation process is developmentally and sex contingent. These findings suggest that effective prevention and intervention for IGD in adolescents with ADHD should incorporate developmentally and sex-sensitive strategies that address peer victimisation and emotional distress in addition to core ADHD symptoms.</p>","PeriodicalId":12549,"journal":{"name":"General Psychiatry","volume":"39 1","pages":"e70012"},"PeriodicalIF":6.8,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13015837/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147520771","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Threshold effects of serum 25-hydroxyvitamin D levels on major depressive symptoms.","authors":"Qinghua Fan, Yi Guo, Zhongjian Liu, Rongtian Xu, Haibo Wang","doi":"10.1002/gps3.70001","DOIUrl":"10.1002/gps3.70001","url":null,"abstract":"","PeriodicalId":12549,"journal":{"name":"General Psychiatry","volume":"39 1","pages":"e70001"},"PeriodicalIF":6.8,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13015814/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147520782","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dementia risk prediction in individuals with prediabetes or diabetes: A novel multi-protein score with biological pathway analysis.","authors":"Yuanyuan Zhang, Yu Huang, Junyu Xue, Yiwei Zhang, Sisi Yang, Yanjun Zhang, Ziliang Ye, Xiaoqin Gan, Yiting Wu, Fanfan Hou, Xianhui Qin","doi":"10.1002/gps3.70010","DOIUrl":"https://doi.org/10.1002/gps3.70010","url":null,"abstract":"<p><strong>Background: </strong>Individuals with prediabetes or diabetes face elevated dementia risk, yet robust prediction tools and mechanistic insights remain limited.</p><p><strong>Aims: </strong>This study aimed to develop and validate a protein-based risk score for dementia prediction in this high-risk population while elucidating underlying biological pathways and therapeutic targets.</p><p><strong>Methods: </strong>Utilising data from 10 433 UK Biobank participants with prediabetes or diabetes and proteomic profiling (2911 plasma proteins measured), we developed a dementia protein risk score in a training set (<i>n</i> = 6514) and validated it in testing (<i>n</i> = 2790) and external cohorts (<i>n</i> = 1129).</p><p><strong>Results: </strong>In the training set, 23 out of 2911 proteins were selected. In the testing set, compared with the basic model (age and sex, C-index: 0.78; 95% confidence interval [CI] 0.74-0.82), the dementia protein risk score (C-index: 0.84; 95% CI 0.81-0.88) significantly improved the performance in predicting incident dementia (C-index increase: 0.06; 95% CI 0.02-0.12), while cardiovascular risk factors, ageing and dementia incidence risk factors (C-index: 0.80; 95% CI 0.76-0.83) and apolipoprotein E (APOE; age and sex included, C-index: 0.81; 95% CI 0.77-0.85) had no significant improvement. Six key proteins (glial fibrillary acidic protein [GFAP], neurofilament light polypeptide [NEFL], Brevican core protein [BCAN], protein MENT [MENT], APOE and growth/differentiation factor 15 [GDF15]) captured the most predictive power. Pathway analyses implicated extracellular matrix remodelling and cholesterol metabolism, whereas Mendelian randomisation identified causal roles for APOE, haematopoietic prostaglandin D synthase (HPGDS), BAG family molecular chaperone regulator 3 (BAG3) and GDF15. Nine proteins were prioritised as druggable targets, including HPGDS, with existing Food and Drug Administration-approved drugs.</p><p><strong>Conclusions: </strong>This study establishes a highly accurate protein-based risk score for dementia prediction (including 6-23 proteins) in individuals with prediabetes or diabetes, uncovering actionable biological pathways and therapeutic targets. The findings enable precision risk stratification and accelerate translational opportunities for dementia prevention in this population.</p>","PeriodicalId":12549,"journal":{"name":"General Psychiatry","volume":"39 1","pages":"e70010"},"PeriodicalIF":6.8,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13015835/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147520789","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}