Schizophrenia Research最新文献

{"title":"Sex versus gender associations with depressive symptom trajectories over 24 months in first-episode schizophrenia spectrum disorders","authors":"H.K. Luckhoff ,&nbsp;E.C. del Re ,&nbsp;R. Smit ,&nbsp;S. Kilian ,&nbsp;L. Phahladira ,&nbsp;R. Emsley ,&nbsp;L. Asmal","doi":"10.1016/j.schres.2024.10.022","DOIUrl":"10.1016/j.schres.2024.10.022","url":null,"abstract":"<div><h3>Background</h3><div>Females with schizophrenia often experience more severe and persistent depressive symptoms than males, in particular during the acute phase of the illness. In contrast to sex (a biological distinction), little is known about the associations between gender (a societal construct) and depression in schizophrenia.</div></div><div><h3>Aim</h3><div>We examined the associations of sex versus gender with visit-wise changes in depressive symptoms over 24 months in patients with first-episode schizophrenia spectrum disorders (FES) (<em>n</em> = 77) compared to matched healthy controls (<em>n</em> = 64).</div></div><div><h3>Methods</h3><div>The Bem Sex Role Inventory was used to measure feminine gender role endorsement. The Calgary Depression Scale for Schizophrenia was used to measure depressive symptoms at baseline, weeks 2, 4, and 6, and months 3, 6, 9, 12, 15, 18, 21, and 24. We used mixed models for continuous repeated measures to examine the moderating effects of childhood trauma, premorbid adjustment, age of psychosis onset, and cannabis use on the associations of sex and gender with depressive symptoms.</div></div><div><h3>Results</h3><div>Higher feminine gender role endorsement, independent of biological sex, was associated with more severe baseline depression and worse initial treatment trajectories. Childhood trauma exposure was also associated with worse depression outcomes, and mediated the association between gender and pre-treatment depression severities.</div></div><div><h3>Conclusions</h3><div>Gender, but not sex, was associated with depressive symptom trajectories in FES. The consideration of both sex and gender offered a more nuanced insight into depressive symptoms compared to biological sex alone.</div></div>","PeriodicalId":21417,"journal":{"name":"Schizophrenia Research","volume":"274 ","pages":"Pages 450-456"},"PeriodicalIF":3.6,"publicationDate":"2024-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142606091","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Meta-analysis of the factor structure of the Scale for the Assessment of Negative Symptoms (SANS) and the Scale for the Assessment of Positive Symptoms (SAPS)","authors":"Federico Dazzi ,&nbsp;Alan Shafer","doi":"10.1016/j.schres.2024.10.027","DOIUrl":"10.1016/j.schres.2024.10.027","url":null,"abstract":"<div><h3>Introduction</h3><div>The SAPS and SANS was designed to measure two broad factors, but the majority of factor analyses conducted have found substantially more dimensions. To investigate their structure a meta-analysis was conducted of SAPS and SANS factor analysis.</div></div><div><h3>Method</h3><div>A total of 42 articles reporting 55 factor analyses were retrieved from database searches (PubMed, PsychINFO) supplemented by searches of references. Reproduced correlations were calculated from retrieved factor analyses and 3 separate meta-analyses were conducted.</div></div><div><h3>Results</h3><div>The meta-analysis of the SAPS SANS global ratings (k = 34; <em>n</em> = 5219) yielded a 3-factor solution including Positive Symptoms (Hallucinations and Delusions), Negative Symptoms (Affective Flattening, Alogia, Avolition/Apathy, Anhedonia/Asociality and Attentional Impairment), and Disorganization (Positive Formal Thought Disorder and Bizarre Behavior). The item analysis of the SAPS SANS combined (k = 11; <em>n</em> = 3146) found 4 factors, with the Negative Symptoms splitting into Affective Flattening/Alogia and Avolition/Asociality as main difference. The SANS only item analysis (k = 10; <em>n</em> = 2073) identified 3 factors, Affective Flattening, Avolition/Asociality, and Alogia/Inattentiveness. Importantly, our data suggests that the items Inappropriate Affect and Poverty of Content of Speech should be moved from Negative Symptoms to the Disorganization factor. Attentional Impairment shows the highest loading on Negative Symptoms but its inclusion under this dimension is conceptually unclear and it may be better considered as a non-specific domain.</div></div><div><h3>Conclusions</h3><div>The three factor structure of Positive Symptoms, Negative Symptoms and Disorganization accounted for most of the data. The SAPS SANS global scales are generally valid, but suggestions for a conservative revision of SAPS SANS structure, including supplementary subscales, are presented.</div></div>","PeriodicalId":21417,"journal":{"name":"Schizophrenia Research","volume":"274 ","pages":"Pages 464-472"},"PeriodicalIF":3.6,"publicationDate":"2024-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142606084","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sleep oscillations and their relations with sleep-dependent memory consolidation in early course psychosis and first-degree relatives","authors":"Dan Denis ,&nbsp;Bengi Baran ,&nbsp;Dimitrios Mylonas ,&nbsp;Courtney Spitzer ,&nbsp;Nicolas Raymond ,&nbsp;Christine Talbot ,&nbsp;Erin Kohnke ,&nbsp;Olivia Larson ,&nbsp;Robert Stickgold ,&nbsp;Matcheri Keshavan ,&nbsp;Dara S. Manoach","doi":"10.1016/j.schres.2024.10.026","DOIUrl":"10.1016/j.schres.2024.10.026","url":null,"abstract":"<div><div>Sleep spindles mediate sleep-dependent memory consolidation, particularly when coupled to neocortical slow oscillations (SOs). Schizophrenia is characterized by a deficit in sleep spindles that correlates with reduced overnight memory consolidation. Here, we examined sleep spindle activity, SO-spindle coupling, and both motor procedural and verbal declarative memory consolidation in early course, minimally medicated psychosis patients and non-psychotic first-degree relatives. Using a four-night experimental procedure, we observed significant deficits in spindle density and amplitude in patients relative to controls that were driven by individuals with schizophrenia. Schizophrenia patients also showed reduced sleep-dependent consolidation of motor procedural memory, which correlated with lower spindle density. Contrary to expectations, there were no group differences in the consolidation of declarative memory on a word pairs task. Nor did the relatives of patients differ in spindle activity or memory consolidation compared with controls, however increased consistency in the timing of SO-spindle coupling were seen in both patients and relatives. Our results extend prior work by demonstrating correlated deficits in sleep spindles and sleep-dependent motor procedural memory consolidation in early course, minimally medicated patients with schizophrenia, but not in first-degree relatives. This is consistent with other work in suggesting that impaired sleep-dependent memory consolidation has some specificity for schizophrenia and is a core feature rather than reflecting the effects of medication or chronicity.</div></div>","PeriodicalId":21417,"journal":{"name":"Schizophrenia Research","volume":"274 ","pages":"Pages 473-485"},"PeriodicalIF":3.6,"publicationDate":"2024-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142606095","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Validation of the Amharic version of Cognitive Assessment Interview (CAI-A) in people with schizophrenia in Ethiopia","authors":"Yohannes Gebreegziabhere ,&nbsp;Kassahun Habatmu ,&nbsp;Matteo Cella ,&nbsp;Atalay Alem","doi":"10.1016/j.schres.2024.10.019","DOIUrl":"10.1016/j.schres.2024.10.019","url":null,"abstract":"<div><div>Assessing cognition with interview-based measures could be a low-resource alternative to traditional cognitive tests. We previously adapted the Cognitive Assessment Interview (CAI) into Amharic (CAI-A) for use with people with schizophrenia (PWS) in Ethiopia. This study examined the convergent and structural validity of the CAI-A in a group of 350 PWS sub-sampled from the Neuropsychiatric Genetics of African Populations – Psychosis (NeuroGAP-Psychosis) study, who fulfilled the inclusion criteria. Data were analyzed using confirmatory factor analysis (CFA), Spearman's correlation coefficient (<em>ρ</em>), multiple regression, and Item Response Theory (IRT). A one-factor solution best fits the items in the tool (factor loadings between 0.58 and 0.79), suggesting structural validity. The total score of the CAI-A moderately correlated with functioning (<em>ρ</em> = 0.44, <em>p</em> &lt; 0.001) and symptom dimensions (<em>ρ</em> between 0.38 and 0.46, <em>p</em> &lt; 0.001), suggesting convergent validity. Multiple regression showed that age (<em>β</em> = −0.06, 95 % CI (−0.12, 0.00), <em>p</em> = 0.044), the duration of illness (<em>β</em> = 0.08, 95 % CI (0.01, 0.14), <em>p</em> = 0.033), and medication side effects (<em>β</em> = 0.35, 95 % CI (0.21, 0.50), <em>p</em> &lt; 0.001) were positively and significantly associated with the CAI-A total score. The IRT analysis suggested that the tool best functions among participants with moderate to severe impairment (difficulty coefficient between 0.05 and 2.73). We found that the CAI-A is a valid tool for use in Ethiopia. The moderate correlation with symptom and functional measures suggested that self-reported cognitive symptoms parallel other symptom dimensions and functional disability. The CAI-A can be used in clinical practice and research activities in PWS in Ethiopia when subjective assessment of cognition is desired.</div></div>","PeriodicalId":21417,"journal":{"name":"Schizophrenia Research","volume":"274 ","pages":"Pages 441-449"},"PeriodicalIF":3.6,"publicationDate":"2024-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142593667","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Intentional non-adherence to antipsychotic medication in patients with schizophrenia","authors":"Hodaka Yaegashi ,&nbsp;Mizuki Haga ,&nbsp;Fuminari Misawa ,&nbsp;Yuya Mizuno ,&nbsp;Takefumi Suzuki ,&nbsp;Hiroyoshi Takeuchi","doi":"10.1016/j.schres.2024.10.018","DOIUrl":"10.1016/j.schres.2024.10.018","url":null,"abstract":"<div><h3>Background</h3><div>Although adherence to antipsychotic medication is critical in the treatment of schizophrenia, prior studies have not adequately distinguished between intentional and unintentional non-adherence.</div></div><div><h3>Methods</h3><div>This study included outpatients with schizophrenia. Self-reported intentional non-adherence was assessed cross-sectionally using the Japanese version of the Intentional Non-Adherence Scale (INAS-J). Item G12 of the Positive and Negative Syndrome Scale (PANSS), Medication Possession Ratio (MPR), psychiatric symptoms, side effects, and medication status were also assessed. An exploratory factor analysis was carried out to examine the factor structure of the INAS. Multiple regression analyses were conducted to examine factors associated with intentional non-adherence.</div></div><div><h3>Results</h3><div>A total of 93 patients were included. The mean ± SD of INAS total score was 36.6 ± 16.2 (out of a maximum score of 110), with 33 subjects (35.5 %) having a minimum score of 22. The mean MPR was 98.2 ± 10.0 %, and the mean score for PANSS G12 was 1.8 ± 1.1. These suggested that they had well-preserved illness insight and good medication adherence. Exploratory factor analysis of the INAS revealed two factors, “Concern about medication” and “Confirming medication need”. No variables were significantly associated with the INAS total score.</div></div><div><h3>Conclusions</h3><div>This is the first study to evaluate intentional non-adherence in patients with schizophrenia. Intentional non-adherence was low in this population. Our findings should be interpreted in the context of patients presenting with relatively well-preserved insight and good medication adherence. Further investigations using the INAS are warranted to examine intentional non-adherence in patients with more diverse backgrounds.</div></div>","PeriodicalId":21417,"journal":{"name":"Schizophrenia Research","volume":"274 ","pages":"Pages 427-432"},"PeriodicalIF":3.6,"publicationDate":"2024-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142586540","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A novel digital intervention for improving cognitive impairment in patients with chronic schizophrenia: A randomized clinical trial","authors":"Lingzi Xu ,&nbsp;Wenjing Yang ,&nbsp;Ruoxin Fan ,&nbsp;Yingying Wu ,&nbsp;Yajing Tang ,&nbsp;Ruobing Zhang ,&nbsp;Xianmei Yang","doi":"10.1016/j.schres.2024.10.023","DOIUrl":"10.1016/j.schres.2024.10.023","url":null,"abstract":"<div><h3>Background</h3><div>There is an unmet need for stand-alone digital therapeutics for cognitive impairment in schizophrenia. This study aimed to evaluate the efficacy and acceptability of a novel digital therapeutic, IBT-SC02, for cognitive impairment in stable schizophrenia patients.</div></div><div><h3>Methods</h3><div>A randomized, parallel-group trial was conducted at the Sichuan Province Institute of Mental Health, China. Participants aged 18–50 diagnosed with schizophrenia were randomized to either the IBT-SC02 intervention or a wait-list control. The primary outcome was cognitive performance measured using the MATRICS Consensus Cognitive Battery (MCCB) composite score.</div></div><div><h3>Results</h3><div>A total of 80 patients were randomized (40 intervention, 40 control). The dropout rate was 5 %. The intervention group exhibited significant improvements in the MCCB composite score compared to the control, though the improvement lessened after excluding data collected by unmasked raters. Post-hoc analyses revealed that participants in the intervention group improved in four out of the seven MCCB domains (speed of processing, verbal learning, visual learning and reasoning and problem solving). No adverse events were reported.</div></div><div><h3>Conclusions</h3><div>These results suggest that IBT-SC02, a fully automated digital therapeutic, improved cognitive performance in patients with stable schizophrenia and can potentially be a treatment option for patients without access to trained professionals.</div></div>","PeriodicalId":21417,"journal":{"name":"Schizophrenia Research","volume":"274 ","pages":"Pages 433-440"},"PeriodicalIF":3.6,"publicationDate":"2024-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142586541","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Modeling common and rare genetic risk factors of neuropsychiatric disorders in human induced pluripotent stem cells","authors":"Abdurrahman W. Muhtaseb ,&nbsp;Jubao Duan","doi":"10.1016/j.schres.2022.04.003","DOIUrl":"10.1016/j.schres.2022.04.003","url":null,"abstract":"<div><div><span><span><span>Recent genome-wide association studies (GWAS) and whole-exome sequencing of neuropsychiatric disorders, especially schizophrenia, have identified a plethora of common and rare disease risk variants/genes. </span>Translating the mounting human </span>genetic discoveries into novel disease biology and more tailored clinical treatments is tied to our ability to causally connect genetic risk variants to molecular and cellular phenotypes. When combined with the </span><u>C</u>lustered <u>R</u>egularly <u>I</u>nterspaced <u>S</u>hort <u>P</u>alindromic <u>R</u><span><span>epeats (CRISPR)/CRISPR-associated (Cas) nuclease-mediated genome editing system, human induced pluripotent stem cell (hiPSC)-derived neural cultures (both 2D and 3D organoids) provide a promising tractable cellular model for bridging the gap between genetic findings and disease biology. In this review, we first conceptualize the advances in understanding the disease polygenicity and convergence from the past decade of iPSC modeling of different types of genetic risk factors of neuropsychiatric disorders. We then discuss the major cell types and cellular phenotypes that are most relevant to neuropsychiatric disorders in iPSC modeling. Finally, we critically review the limitations of iPSC modeling of neuropsychiatric disorders and outline the need for implementing and developing novel methods to </span>scale up the number of iPSC lines and disease risk variants in a systematic manner. Sufficiently scaled-up iPSC modeling and a better functional interpretation of genetic risk variants, in combination with cutting-edge CRISPR/Cas9 gene editing and single-cell multi-omics methods, will enable the field to identify the specific and convergent molecular and cellular phenotypes in precision for neuropsychiatric disorders.</span></div></div>","PeriodicalId":21417,"journal":{"name":"Schizophrenia Research","volume":"273 ","pages":"Pages 39-61"},"PeriodicalIF":3.6,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10744336","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cell line specific alterations in genes associated with dopamine metabolism and signaling in midbrain dopaminergic neurons derived from 22q11.2 deletion carriers with elevated dopamine synthesis capacity","authors":"Matthew J. Reid ,&nbsp;Maria Rogdaki ,&nbsp;Lucia Dutan ,&nbsp;Bjørn Hanger ,&nbsp;Kaarin Sabad ,&nbsp;Roland Nagy ,&nbsp;Dwaipayan Adhya ,&nbsp;Simon Baron-Cohen ,&nbsp;Grainne McAlonan ,&nbsp;Jack Price ,&nbsp;Anthony C. Vernon ,&nbsp;Oliver D. Howes ,&nbsp;Deepak P. Srivastava","doi":"10.1016/j.schres.2022.05.010","DOIUrl":"10.1016/j.schres.2022.05.010","url":null,"abstract":"<div><div>Microdeletions at the 22q11.2 locus are associated with increased risk for schizophrenia. Recent work has demonstrated that antipsychotic naïve 22q11.2 carriers display elevated levels of dopamine synthesis capacity (DSC) as assessed by ¹⁸F-DOPA PET imaging. While this is consistent with a role for abnormal dopamine function in schizophrenia, it is unclear what molecular changes may be associated with this neuro-imaging endophenotype, and moreover, if these alterations occur independently of clinical presentation. We therefore conducted a pilot study in which we generated human induced pluripotent stem cells (hiPSCs) from two 22q11.2 deletion carriers with elevated DSC <em>in vivo</em>, but distinct clinical presentations. From these and neurotypical control lines we were able to robustly generate midbrain dopaminergic neurons (mDA-neurons). We then assessed whether genes associated with dopamine synthesis, metabolism or signaling show altered expression between genotypes and further between the 22q11.2 deletion lines. Our data showed alterations in expression of genes associated with dopamine metabolism and signaling that differed between the two 22q11.2 hiPSC lines with distinct clinical presentations. This reinforces the importance of considering clinical, genetic and molecular information, when possible, when choosing which donors to generate hiPSCs from, to carry out mechanistic studies.</div></div>","PeriodicalId":21417,"journal":{"name":"Schizophrenia Research","volume":"273 ","pages":"Pages 98-106"},"PeriodicalIF":3.6,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9105944","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Probing the biological consequences of a previously undescribed de novo mutation of ZMYND11 in a schizophrenia patient by CRISPR genome editing and induced pluripotent stem cell based in vitro disease-modeling","authors":"Csongor Tordai ,&nbsp;Edit Hathy ,&nbsp;Hella Gyergyák ,&nbsp;Katalin Vincze ,&nbsp;Máté Baradits ,&nbsp;Júlia Koller ,&nbsp;Ádám Póti ,&nbsp;Bálint Jezsó ,&nbsp;László Homolya ,&nbsp;Mária Judit Molnár ,&nbsp;László Nagy ,&nbsp;Dávid Szüts ,&nbsp;Ágota Apáti ,&nbsp;János M. Réthelyi","doi":"10.1016/j.schres.2024.01.024","DOIUrl":"10.1016/j.schres.2024.01.024","url":null,"abstract":"<div><h3>Background</h3><div>Schizophrenia (SCZ) is a severe neuropsychiatric disorder of complex, poorly understood etiology, associated with both genetic and environmental factors. De novo mutations (DNMs) represent a new source of genetic variation in SCZ, however, in most cases their biological significance remains unclear. We sought to investigate molecular disease pathways connected to DNMs in SCZ by combining human induced pluripotent stem cell (hiPSC) based disease modeling and CRISPR-based genome editing.</div></div><div><h3>Methods</h3><div>We selected a SCZ case-parent trio with the case individual carrying a potentially disease causing 1495C &gt; T nonsense DNM in the zinc finger MYND domain-containing protein 11 (ZMYND11), a gene implicated in biological processes relevant for SCZ. In the patient-derived hiPSC line the mutation was corrected using CRISPR, while monoallelic or biallelic frameshift mutations were introduced into a control hiPSC line. Isogenic cell lines were differentiated into hippocampal neuronal progenitor cells (NPCs) and functionally active dentate gyrus granule cells (DGGCs). Immunofluorescence microscopy and RNA sequencing were used to test for morphological and transcriptomic differences at NPC and DGCC stages. Functionality of neurons was investigated using calcium-imaging and multi-electrode array measurements.</div></div><div><h3>Results</h3><div>Morphology in the mutant hippocampal NPCs and neurons was preserved, however, we detected significant transcriptomic and functional alterations. RNA sequencing showed massive upregulation of neuronal differentiation genes, and downregulation of cell adhesion genes. Decreased reactivity to glutamate was demonstrated by calcium-imaging.</div></div><div><h3>Conclusions</h3><div>Our findings lend support to the involvement of glutamatergic dysregulation in the pathogenesis of SCZ. This approach represents a powerful model system for precision psychiatry and pharmacological research.</div></div>","PeriodicalId":21417,"journal":{"name":"Schizophrenia Research","volume":"273 ","pages":"Pages 107-120"},"PeriodicalIF":3.6,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139591756","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mitochondrial dysfunction in psychiatric disorders","authors":"Peiyan Ni ,&nbsp;Yao Ma ,&nbsp;Sangmi Chung","doi":"10.1016/j.schres.2022.08.027","DOIUrl":"10.1016/j.schres.2022.08.027","url":null,"abstract":"<div><div>Psychiatric disorders are a heterogeneous group of mental disorders with abnormal mental or behavioral patterns, which severely distress or disable affected individuals and can have a grave socioeconomic burden. Growing evidence indicates that mitochondrial function plays an important role in developing psychiatric disorders. This review discusses the neuropsychiatric consequences of mitochondrial abnormalities in both animal models and patients. We also discuss recent studies associated with compromised mitochondrial function in various psychiatric disorders, such as schizophrenia (SCZ), major depressive disorder (MD), and bipolar disorders (BD). These studies employ various approaches including postmortem studies, imaging studies, genetic studies, and induced pluripotent stem cells (iPSCs) studies. We also summarize the evidence from animal models and clinical trials to support mitochondrial function as a potential therapeutic target to treat various psychiatric disorders. This review will contribute to furthering our understanding of the metabolic etiology of various psychiatric disorders, and help guide the development of optimal therapies.</div></div>","PeriodicalId":21417,"journal":{"name":"Schizophrenia Research","volume":"273 ","pages":"Pages 62-77"},"PeriodicalIF":3.6,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40382477","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}