Molecular Psychiatry最新文献

{"title":"Astrocyte morphological remodeling regulates consciousness state transitions induced by inhaled general anesthesia","authors":"Bin Zhou, Qingran Li, Mengchan Su, Ping Liao, Yuncheng Luo, Rong Luo, Yunqing Yu, Meiyan Luo, Fan Lei, Xin Li, Jiao Jiao, Limei Yi, Jing Wang, Linghui Yang, Daqing Liao, Cheng Zhou, Xia Zhang, Hong Xiao, Yunxia Zuo, Jin Liu, Tao Zhu, Ruotian Jiang","doi":"10.1038/s41380-025-02978-2","DOIUrl":"https://doi.org/10.1038/s41380-025-02978-2","url":null,"abstract":"<p>General anesthetics (GAs) are conventionally thought to induce loss of consciousness (LOC) by acting on pre- and post-synaptic targets. However, the mechanism underlying the involvement of astrocytes in LOC remains unclear. Here we report that inhaled GAs cause reversible impairments in the fine processes of astrocytes within the somatosensory cortex, mediated by regulating the phosphorylation level of Ezrin, a protein critical for the fine morphology of astrocytes. Genetically deleting Ezrin or disrupting its phosphorylation was sufficient to decrease astrocyte-synapse interaction and enhance sensitivity to sevoflurane (Sevo) in vivo. Moreover, we show that disrupting astrocytic Ezrin phosphorylation boosted the inhibitory effect of Sevo on pyramidal neurons by enhancing tonic GABA and lowering excitability under anesthesia. Our work reveals previously unappreciated phosphorylation-dependent morphological dynamics, which enable astrocytes to regulate neuronal activity during the transition between two brain consciousness states.</p><figure></figure>","PeriodicalId":19008,"journal":{"name":"Molecular Psychiatry","volume":"22 1","pages":""},"PeriodicalIF":11.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143744879","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Differential impact of cerebral small vessel disease on thalamic regulation of anxiety: insights from 7T MRI","authors":"Bei Wang, Cen Guo, Ying-Hua Chu, Yajing Huo, Boyu Zhang, Guanshu Liu, Yan Han, He Wang","doi":"10.1038/s41380-025-02994-2","DOIUrl":"https://doi.org/10.1038/s41380-025-02994-2","url":null,"abstract":"<p>Little is known about how thalamic vascular patterns interact with small vessel diseases (SVDs) to influence affective symptoms. Here we collected 7-Telsa magnetic resonance imaging (MRI) data from 84 individuals with SVD and analyzed the influences of thalamic vascular pattern on affective symptoms, aiming to elucidate the underlying mechanisms driven by brain structure and function in the context of SVD. Subjects with a combined arterial supply by tuberothalamic and paramedian arteries to the right thalamus exhibited a lower Hamilton Anxiety scale (HAMA) score. When grouped by SVD burden, the same correlation remained in subjects with low SVD burden, whereas no difference was observed in the high SVD burden group. Interestingly, interaction effects of SVD and thalamic vascular pattern were also found affecting thalamic volume and resting-state brain activity in ventromedial prefrontal cortex (vmPFC). With moderated mediation analysis, right thalamic vascular pattern was indicated to affect anxiety through both direct (vascular pattern → HAMA score) and indirect (vascular pattern → thalamic volume → HAMA score) pathways. But high SVD burden interrupted the effects of right thalamic vascular pattern on HAMA score and thalamic volume. The finding that subjects with a combined arterial supply to the right thalamus exhibited a lower level of anxiety may suggest a novel vascular resilience for regulating anxiety. However, this vascular compensation mechanism was found to be impaired by elevated SVD burden and the disrupted inhibitory vmPFC activity caused by impaired thalamus. The findings of the present study provide a new underlying mechanism for affective disorders with SVD involved.</p>","PeriodicalId":19008,"journal":{"name":"Molecular Psychiatry","volume":"32 1","pages":""},"PeriodicalIF":11.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143758094","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association between the childhood rearing environment and general and specific psychopathology factors in middle adulthood: a Swedish National High-Risk Home-Reared versus Adopted-Away Sibling Comparison Study","authors":"Mengping Zhou, Henrik Larsson, Brian M. D’Onofrio, Mikael Landén, Paul Lichtenstein, Erik Pettersson","doi":"10.1038/s41380-025-02979-1","DOIUrl":"https://doi.org/10.1038/s41380-025-02979-1","url":null,"abstract":"<p>Quasi-experimental and randomized controlled studies suggest that an enriched childhood rearing environment for at-risk individuals can reduce the risk for several psychiatric conditions. However, it remains uncertain if the reduced risk might be attributable to a general psychopathology factor common to all psychiatric conditions, versus specific psychopathology factors unique to only subsets of psychiatric conditions. In an at-risk sample, we estimated the association between an enriched childhood rearing environment and a latent bifactor model that captured both general and several specific psychopathology factors. The sample consisted of 881 full sibships where (a) the biological parents had (at least) one psychiatric diagnosis, suicide, or crime at any time in their lives, and (b) where (at least) one sibling was adopted away and raised by non-biological parents and (at least) one sibling raised by the biological parents. The exposure was whether a sibling was raised by biological versus adoptive parents. The outcome was a latent bifactor model based on nine conditions, including 7 in- or outpatient psychiatric diagnoses, suicide, and crimes. We recorded these outcomes from the birth of the siblings until the end of 2013, when the siblings were 34–64 years old. We used the marginal between-within model to estimate whether the adopted-away sibling(s) had lower scores on the latent factors. The latent bifactor model based on the nine conditions consisted of one general and three specific (externalizing, internalizing, and psychotic) psychopathology factors. The adopted-away siblings scored 0.27 (95% CI: −0.36, −0.18) standard deviations lower on the latent general psychopathology factor and 0.26 (95% CI: −0.38, −0.14) standard deviations lower on the latent specific externalizing factor, compared to their biological siblings who were raised by the biological parents. This result indicates that although genetics appears important for psychiatric comorbidity, the rearing environment also appears to play a systematic role in influencing the liability toward all mental health conditions among at-risk individuals. Improving the childhood rearing environment in high-risk families could potentially mitigate children’s liability toward all psychiatric conditions.</p>","PeriodicalId":19008,"journal":{"name":"Molecular Psychiatry","volume":"15 1","pages":""},"PeriodicalIF":11.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143744881","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Higher plasma soluble TREM2 correlates with reduced cerebral tau accumulation in Alzheimer’s disease","authors":"Guoyu Lan, Anqi Li, Fernando Gonzalez-Ortiz, Jieqin Lv, Wenqing Ran, Yue Cai, Pan Sun, Lin Liu, Jie Yang, Laihong Zhang, Zhengbo He, Lili Fang, Xin Zhou, Yalin Zhu, Zhen Liu, Xiang Fan, Xuhui Chen, Linsen Xu, Qingyong Wang, Xinlu Wang, Kun Sun, Guanxun Cheng, Ying Han, Kaj Blennow, Lu Wang, Pengcheng Ran, Tengfei Guo","doi":"10.1038/s41380-025-02976-4","DOIUrl":"https://doi.org/10.1038/s41380-025-02976-4","url":null,"abstract":"<p>Loss-of-function mutation of triggering receptor expressed on myeloid cell 2 (TREM2) is associated with increased risks for Alzheimer’s disease (AD). Recent animal studies reveal that the activation of peripheral TREM2 signaling may affect cerebral β-amyloid (Aβ) and tau aggregates. However, the underlying relationship between peripheral TREM2 and brain AD pathology has not yet been well-elucidated in the aging population. In this study, we collected 318 Chinese older adults with Aβ PET and plasma biomarker measures, including soluble TREM2 (sTREM2) and glial fibrillary acidic protein (GFAP), a proxy for astrocyte reactivity. Additionally, 129 participants underwent tau PET scans. We explored the association between plasma sTREM2, GFAP, and primary AD pathology. Plasma sTREM2 was negatively associated with reduced temporal tau PET burden in participants with abnormal Aβ and tau pathology. Higher plasma sTREM2 was related to the weaker association of Aβ pathology and plasma phosphorylated tau with tau PET increases. In contrast, elevated plasma GFAP was related to greater Aβ and tau PET burden along with stronger Aβ-related tau accumulation. Finally, higher plasma sTREM2 was linked to attenuated strength of the association between plasma GFAP and tau PET increases at both pre-defined regions of interest and voxel levels. Altogether, our findings suggest distinct relationships between plasma sTREM2 and GFAP with cerebral tau pathology, providing novel insights into the roles of peripheral TREM2 signaling and astrocytic reactivity in AD neuropathological development. This study has important implications, such as targeting the peripheral TREM2 signature, which may be a potential strategy for future AD therapies.</p>","PeriodicalId":19008,"journal":{"name":"Molecular Psychiatry","volume":"12 1","pages":""},"PeriodicalIF":11.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143744880","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mutation of CHD7 impairs the output of neuroepithelium transition that is reversed by the inhibition of EZH2","authors":"Zhuxi Huang, Chenxi He, Guangfu Wang, Ming Zhu, Xiaoyu Tong, Yi Feng, Chenyang Zhang, Shuhua Dong, Yassin Harim, Hai-kun Liu, Wenhao Zhou, Fei Lan, Weijun Feng","doi":"10.1038/s41380-025-02990-6","DOIUrl":"https://doi.org/10.1038/s41380-025-02990-6","url":null,"abstract":"<p>Haploinsufficiency of <i>CHD7</i> (Chromo-Helicase-DNA binding protein 7) causes a severe congenital disease CHARGE syndrome. Brain anomaly such as microcephaly and olfactory bulb agenesis seen in CHARGE patients have not been mimicked in previous animal models. Here, we uncover an indispensable function of <i>CHD7</i> in the neuroepithelium (NE) but not in the neural stem cells (NSCs) after NE transition. Loss of <i>Chd7</i> in mouse NE resulted in CHARGE-like brain anomalies due to reduced proliferation and differentiation of neural stem and progenitor cells, which were recapitulated in <i>CHD7</i> KO human forebrain organoids. Mechanistically, we find that CHD7 activates neural transcription factors by removing the repressive histone mark H3K27me3 and promoting chromatin accessibility. Importantly, neurodevelopmental defects caused by <i>CHD7</i> loss in human brain organoids and mice were ameliorated by the inhibition of H3K27me3 methyltransferase EZH2. Altogether, by implementing appropriate experimental models, we uncover the pathogenesis of <i>CHD7</i>-associated neurodevelopmental diseases, and identify a potential therapeutic opportunity for CHARGE syndrome.</p>","PeriodicalId":19008,"journal":{"name":"Molecular Psychiatry","volume":"56 1","pages":""},"PeriodicalIF":11.0,"publicationDate":"2025-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143744883","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cholinergic tone abnormalities and relationships with smoking severity in human cigarette smokers: exploratory positron emission tomography study using [18F]VAT","authors":"Scott J. Moeller, Jodi J. Weinstein, Benjamin Varnas, Olivia Orellano, Roberto Gil, Greg Perlman, Sameera Abeykoon, Jiayan Meng, Ingrid Oprea, Bao Hu, Wenchao Qu, Mark Slifstein, Anissa Abi-Dargham","doi":"10.1038/s41380-025-02985-3","DOIUrl":"https://doi.org/10.1038/s41380-025-02985-3","url":null,"abstract":"<p>Nicotine acts on the brain cholinergic system to drive the rewarding effects of cigarettes and perpetuate smoking. Prior studies in human smokers have used positron emission tomography (PET) to characterize differences in postsynaptic nicotinic acetylcholine receptors (nAChRs). However, preclinical studies indicate that nicotine also modulates presynaptic cholinergic targets that have implications for transmission, including the vesicular acetylcholine transporter (VAChT). To date, there is a paucity of studies imaging presynaptic targets in human smokers. We conducted an initial PET neuroimaging study with [¹⁸F]VAT, which indexes VAChT availability (presynaptic marker of cholinergic tone), in 12 healthy smokers and 13 demographically-matched healthy non-smokers. We tested for group differences in VAChT availability, measured as total distribution volume (V_T), in the striatum (main region of interest) and in multiple cortical and subcortical extrastriatal regions. Within smokers, we also tested correlations between VAChT availability and indices of smoking chronicity and tobacco self-administration. Smokers had higher [¹⁸F]VAT V_T than non-smokers in multiple cortical and subcortical regions (<i>p</i> &lt; 0.05_uncorrected). There were no group differences in the striatum. Within smokers, V_T in the dorsolateral prefrontal and temporal cortices was positively correlated with smoking chronicity (<i>p</i> &lt; 0.05_corrected). This study provides first-line evidence of presynaptic cholinergic differences between smokers and non-smokers, such that VAChT is upregulated in smokers and associated with chronicity. Future studies with larger samples are needed to verify these initial effects. With confirmation, these findings could inform the development of new VAChT-targeting therapeutics that could potentially benefit smokers who have been unable to quit with currently available treatments.</p>","PeriodicalId":19008,"journal":{"name":"Molecular Psychiatry","volume":"52 1","pages":""},"PeriodicalIF":11.0,"publicationDate":"2025-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143736628","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metagenomic analysis characterizes stage-specific gut microbiota in Alzheimer’s disease","authors":"Longhao Jia, Yize Ke, Shuo Zhao, Jinxin Liu, Xiaohui Luo, Jixin Cao, Yujia Liu, Qihao Guo, Wei‑Hua Chen, Feng Chen, Jiao Wang, Hao Wu, Jing Ding, Xing‑Ming Zhao","doi":"10.1038/s41380-025-02973-7","DOIUrl":"https://doi.org/10.1038/s41380-025-02973-7","url":null,"abstract":"<p>Alzheimer’s disease (AD) is a progressive neurodegenerative disorder with a decade-long preclinical pathological period that can be divided into several stages. Emerging evidence has revealed that the microbiota-gut-brain axis plays an important role in AD pathology. However, the role of gut microbiota in different AD stages has not been well characterized. In this study, we performed fecal shotgun metagenomic analysis on a Chinese cohort with 476 participants across five stages of AD pathology to characterize stage-specific alterations in gut microbiota and evaluate their diagnostic potential. We discovered extensive gut dysbiosis that is associated with neuroinflammation and neurotransmitter dysregulation, with over 10% of microbial species and gene families showing significant alterations during AD progression. Furthermore, we demonstrated that microbial gene families exhibited strong diagnostic capabilities, evidenced by an average AUC of 0.80 in cross-validation and 0.75 in independent external validation. In the optimal model, the most discriminant gene families are primarily involved in the metabolism of carbohydrates, amino acids, energy, glycan and vitamins. We found that stage-specific microbial gene families in AD pathology could be validated by an in vitro gut simulator and were associated with specific genera. We also observed that the gut microbiota could affect the progression of cognitive decline in 5xFAD mice through fecal microbiota transplantation, which could be used for early intervention of AD. Our multi-stage large cohort metagenomic analysis demonstrates that alterations in gut microbiota occur from the very early stages of AD pathology, offering important etiological and diagnostic insights.</p>","PeriodicalId":19008,"journal":{"name":"Molecular Psychiatry","volume":"8 1","pages":""},"PeriodicalIF":11.0,"publicationDate":"2025-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143744882","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Deep graph learning of multimodal brain networks defines treatment-predictive signatures in major depression","authors":"Yong Jiao, Kanhao Zhao, Xinxu Wei, Nancy B. Carlisle, Corey J. Keller, Desmond J. Oathes, Gregory A. Fonzo, Yu Zhang","doi":"10.1038/s41380-025-02974-6","DOIUrl":"https://doi.org/10.1038/s41380-025-02974-6","url":null,"abstract":"<p>Major depressive disorder (MDD) presents a substantial health burden with low treatment response rates. Predicting antidepressant efficacy is challenging due to MDD’s complex and varied neuropathology. Identifying biomarkers for antidepressant treatment requires thorough analysis of clinical trial data. Multimodal neuroimaging, combined with advanced data-driven methods, can enhance our understanding of the neurobiological processes influencing treatment outcomes. To address this, we analyzed resting-state fMRI and EEG connectivity data from 130 patients treated with sertraline and 135 patients with placebo from the Establishing Moderators and Biosignatures of Antidepressant Response in Clinical Care (EMBARC) study. A deep learning framework was developed using graph neural networks to integrate data-augmented connectivity and cross-modality correlation, aiming to predict individual symptom changes by revealing multimodal brain network signatures. The results showed that our model demonstrated promising prediction accuracy, with an R² value of 0.24 for sertraline and 0.20 for placebo. It also exhibited potential in transferring predictions using only EEG. Key brain regions identified for predicting sertraline response included the inferior temporal gyrus (fMRI) and posterior cingulate cortex (EEG), while for placebo response, the precuneus (fMRI) and supplementary motor area (EEG) were critical. Additionally, both modalities identified the superior temporal gyrus and posterior cingulate cortex as significant for sertraline response, while the anterior cingulate cortex and postcentral gyrus were common predictors in the placebo arm. Additionally, variations in the frontoparietal control, ventral attention, dorsal attention, and limbic networks were notably associated with MDD treatment. By integrating fMRI and EEG, our study established novel multimodal brain network signatures to predict individual responses to sertraline and placebo in MDD, providing interpretable neural circuit patterns that may guide future targeted interventions. Trial Registration: Establishing Moderators and Biosignatures of Antidepressant Response for Clinical Care for Depression (EMBARC) ClinicalTrials.gov Identifier: NCT#01407094.</p>","PeriodicalId":19008,"journal":{"name":"Molecular Psychiatry","volume":"37 1","pages":""},"PeriodicalIF":11.0,"publicationDate":"2025-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143744821","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PD-L1/PD-1 checkpoint pathway regulates astrocyte morphogenesis and myelination during brain development","authors":"Yanyan Wang, Mengtian Zhang, Tianyu Zhang, Shukui Zhang, Fen Ji, Jie Qin, Hong Li, Jianwei Jiao","doi":"10.1038/s41380-025-02969-3","DOIUrl":"https://doi.org/10.1038/s41380-025-02969-3","url":null,"abstract":"<p>Programmed cell death protein 1 (PD-1) and its primary ligand PD-L1 are integral components of a significant immune checkpoint pathway, widely recognized for its central role in cancer immunotherapy. However, emerging evidence highlights their broader involvement in both the central and peripheral nervous systems. In this study, we demonstrate that PD-L1/PD-1 signaling in astrocytes during mouse brain development regulates astrocyte maturation and morphogenesis via the MEK/ERK pathway by targeting the downstream effector cysteine and glycine rich protein 1 (CSRP1). This enhanced astrocyte morphological complexity results in increased end-foot coverage of blood vessels. Additionally, aberrant secretion of CSRP1 by astrocytes interacts with oligodendrocyte precursor cells (OPCs) membrane proteins annexin A1 (ANXA1) and annexin A2 (ANXA2), leading to the exclusion of migrating OPCs from blood vessels. This disruption in OPC migration and differentiation results in abnormal myelination and is associated with cognitive deficits in the mice. Our results provide critical insights into the function of PD-L1/PD-1 signaling in astrocyte-OPC interactions and underscore its relevance to glial cell development and pathogenesis in neurodevelopmental disorders.</p>","PeriodicalId":19008,"journal":{"name":"Molecular Psychiatry","volume":"5 1","pages":""},"PeriodicalIF":11.0,"publicationDate":"2025-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143744822","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: Investigating dopaminergic abnormalities in schizophrenia and first-episode psychosis with normative modelling and multisite molecular neuroimaging.","authors":"Alessio Giacomel, Daniel Martins, Giovanna Nordio, Rubaida Easmin, Oliver Howes, Pierluigi Selvaggi, Steven C R Williams, Federico Turkheimer, Marius De Groot, Ottavia Dipasquale, Mattia Veronese","doi":"10.1038/s41380-025-02987-1","DOIUrl":"https://doi.org/10.1038/s41380-025-02987-1","url":null,"abstract":"","PeriodicalId":19008,"journal":{"name":"Molecular Psychiatry","volume":" ","pages":""},"PeriodicalIF":9.6,"publicationDate":"2025-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143753571","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}