Genes Brain and Behavior最新文献

{"title":"Correction to “Anxiety-related defensive behavioral responses in mice selectively bred for High and Low Activity”","authors":"","doi":"10.1111/gbb.12897","DOIUrl":"10.1111/gbb.12897","url":null,"abstract":"<p>Winona C. Booher, Lucy A. Hall, Aimee L. Thomas, et al. <i>Genes Brain Behav</i>. 2021;e12730.</p><p>In the above article, incorrect versions of Figures 4 and 5 were published in error. In both figures, the Low Activity (dotted line) should be on top and the High Activity (solid line) should be on the bottom.</p><p>The correct figures are reproduced below.</p><p>We apologize for this error.</p>","PeriodicalId":50426,"journal":{"name":"Genes Brain and Behavior","volume":"23 3","pages":""},"PeriodicalIF":2.5,"publicationDate":"2024-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/gbb.12897","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140913239","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Memory, mood and associated neuroanatomy in individuals with steroid sulphatase deficiency (X-linked ichthyosis)","authors":"Georgina H. Wren,&nbsp;Jessica Flanagan,&nbsp;Jack F. G. Underwood,&nbsp;Andrew R. Thompson,&nbsp;Trevor Humby,&nbsp;William Davies","doi":"10.1111/gbb.12893","DOIUrl":"https://doi.org/10.1111/gbb.12893","url":null,"abstract":"<p>Steroid sulphatase (STS) cleaves sulphate groups from steroid hormones, and steroid (sulphate) levels correlate with mood and age-related cognitive decline. In animals, STS inhibition or deletion of the associated gene, enhances memory/neuroprotection and alters hippocampal neurochemistry. Little is known about the consequences of constitutive STS deficiency on memory-related processes in humans. We investigated self-reported memory performance (Multifactorial Memory Questionnaire), word-picture recall and recent mood (Kessler Psychological Distress Scale, K10) in adult males with STS deficiency diagnosed with the dermatological condition X-linked ichthyosis (XLI; <i>n</i> = 41) and in adult female carriers of XLI-associated genetic variants (<i>n</i> = 79); we compared results to those obtained from matched control subjects [diagnosed with ichthyosis vulgaris (IV, <i>n</i> = 98) or recruited from the general population (<i>n</i> = 250)]. Using the UK Biobank, we compared mood/memory-related neuroanatomy in carriers of genetic deletions encompassing <i>STS</i> (<i>n</i> = 28) and non-carriers (<i>n</i> = 34,522). We found poorer word-picture recall and lower perceived memory abilities in males with XLI and female carriers compared with control groups. XLI-associated variant carriers and individuals with IV reported more adverse mood symptoms, reduced memory contentment and greater use of memory aids, compared with general population controls. Mood and memory findings appeared largely independent. Neuroanatomical analysis only indicated a nominally-significantly larger molecular layer in the right hippocampal body of deletion carriers relative to non-carriers. In humans, constitutive STS deficiency appears associated with mood-independent impairments in memory but not with large effects on underlying brain structure; the mediating psychobiological mechanisms might be explored further in individuals with XLI and in new mammalian models lacking STS developmentally.</p>","PeriodicalId":50426,"journal":{"name":"Genes Brain and Behavior","volume":"23 3","pages":""},"PeriodicalIF":2.5,"publicationDate":"2024-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/gbb.12893","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140826149","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Differentially expressed genes of esophageal tissue in male acute and chronic sleep deprivation mice","authors":"Jing Li,&nbsp;Yifan Lu,&nbsp;Dingding Yang,&nbsp;Mudan Ren,&nbsp;Yan Yin,&nbsp;Yan Zhao,&nbsp;Shuixiang He","doi":"10.1111/gbb.12896","DOIUrl":"https://doi.org/10.1111/gbb.12896","url":null,"abstract":"<p>Gastroesophageal reflux disease (GERD) is associated with sleep disturbances. However, mechanisms underlying these interactions remain unclear. Male acute and chronic sleep deprivation (SD) mice were used for this study. Mice in the chronic SD group exhibited anxiety- and depression-like behaviors. We further performed high-throughput genome sequencing and bioinformatics analysis to screen for featured differentially expressed genes (DEGs) in the esophageal tissue. The acute SD group, comprised 25 DEGs including 14 downregulated and 11 upregulated genes. Compared with the acute SD group, more DEGs were present in the chronic SD group, with a total of 169 DEGs, including 88 downregulated and 81 upregulated genes. Some DEGs that were closely related to GERD and associated esophageal diseases were significantly different in the chronic SD group. Quantitative real-time polymerase chain reaction verified the downregulation of Krt4, Krt13, Krt15 and Calml3 and upregulation of Baxl1 and Per3. Notably, these DEGs are involved in biological processes, which might be the pathways of the neuroregulatory mechanisms of DEGs expression.</p>","PeriodicalId":50426,"journal":{"name":"Genes Brain and Behavior","volume":"23 2","pages":""},"PeriodicalIF":2.5,"publicationDate":"2024-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/gbb.12896","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140643438","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genetic background and sex influence somatosensory sensitivity and oxycodone analgesia in the Hybrid Rat Diversity Panel","authors":"Eamonn P. Duffy,&nbsp;J. O. Ward,&nbsp;L. H. Hale,&nbsp;K. T. Brown,&nbsp;Andrew J. Kwilasz,&nbsp;Laura M. Saba,&nbsp;Marissa A. Ehringer,&nbsp;Ryan K. Bachtell","doi":"10.1111/gbb.12894","DOIUrl":"https://doi.org/10.1111/gbb.12894","url":null,"abstract":"<p>Opioid use disorder (OUD) is an ongoing public health concern in the United States, and relatively little work has addressed how genetic background contributes to OUD. Understanding the genetic contributions to oxycodone-induced analgesia could provide insight into the early stages of OUD development. Here, we present findings from a behavioral phenotyping protocol using several inbred strains from the Hybrid Rat Diversity Panel. Our behavioral protocol included a modified “up-down” von Frey procedure to measure inherent strain differences in the sensitivity to a mechanical stimulus on the hindpaw. We also performed the tail immersion assay, which measures the latency to display tail withdrawal in response to a hot water bath. Initial withdrawal thresholds were taken in drug-naïve animals to record baseline thermal sensitivity across the strains. Oxycodone-induced analgesia was measured after administration of oxycodone over the course of 2 h. Both mechanical and thermal sensitivity are shaped by genetic factors and display moderate heritability (<i>h</i>^<i>2</i> = 0.23–0.40). All strains displayed oxycodone-induced analgesia that peaked at 15–30 min and returned to baseline by 2 h. There were significant differences between the strains in the magnitude and duration of their analgesic response to oxycodone, although the heritability estimates were quite modest (<i>h</i>² = 0.10–0.15). These data demonstrate that genetic background confers differences in mechanical sensitivity, thermal sensitivity, and oxycodone-induced analgesia.</p>","PeriodicalId":50426,"journal":{"name":"Genes Brain and Behavior","volume":"23 2","pages":""},"PeriodicalIF":2.5,"publicationDate":"2024-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/gbb.12894","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140541155","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chd8 haploinsufficiency impacts rearing experience in C57BL/6 mice","authors":"Manal Tabbaa,&nbsp;Pat Levitt","doi":"10.1111/gbb.12892","DOIUrl":"https://doi.org/10.1111/gbb.12892","url":null,"abstract":"<p>Mutations in <i>CHD8</i> are one of the highest genetic risk factors for autism spectrum disorder. Studies in mice that investigate underlying mechanisms have shown <i>Chd8</i> haploinsufficient mice display some trait disruptions that mimic clinical phenotypes, although inconsistencies have been reported in some traits across different models on the same strain background. One source of variation across studies may be the impact of <i>Chd8</i> haploinsufficiency on maternal-offspring interactions. While differences in maternal care as a function of <i>Chd8</i> genotype have not been studied directly, a previous study showed that pup survival was reduced when reared by <i>Chd8</i> heterozygous dams compared with wild-type (WT) dams, suggesting altered maternal care as a function of <i>Chd8</i> genotype. Through systematic observation of the C57BL/6 strain, we first determined the impact of <i>Chd8</i> haploinsufficiency in the offspring on WT maternal care frequencies across preweaning development. We next determined the impact of maternal <i>Chd8</i> haploinsufficiency on pup care. Compared with litters with all WT offspring, WT dams exhibited less frequent maternal behaviors toward litters consisting of offspring with mixed <i>Chd8</i> genotypes, particularly during postnatal week 1. Dam <i>Chd8</i> haploinsufficiency decreased litter survival and increased active maternal care also during postnatal week 1. Determining the impact of <i>Chd8</i> haploinsufficiency on early life experiences provides an important foundation for interpreting offspring outcomes and determining mechanisms that underlie heterogeneous phenotypes.</p>","PeriodicalId":50426,"journal":{"name":"Genes Brain and Behavior","volume":"23 2","pages":""},"PeriodicalIF":2.5,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/gbb.12892","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140333079","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Network-based analysis predicts interacting genetic modifiers from a meta-mapping study of spike–wave discharge in mice","authors":"Montana Kay Lara,&nbsp;Jeffrey L. Brabec,&nbsp;Amanda E. Hernan,&nbsp;Rod C. Scott,&nbsp;Anna L. Tyler,&nbsp;J. Matthew Mahoney","doi":"10.1111/gbb.12879","DOIUrl":"10.1111/gbb.12879","url":null,"abstract":"<p>Absence seizures are characterized by brief lapses in awareness accompanied by a hallmark spike-and-wave discharge (SWD) electroencephalographic pattern and are common to genetic generalized epilepsies (GGEs). While numerous genes have been associated with increased risk, including some Mendelian forms with a single causal allele, most cases of GGE are idiopathic and there are many unknown genetic modifiers of GGE influencing risk and severity. In a previous meta-mapping study, crosses between transgenic C57BL/6 and C3HeB/FeJ strains, each carrying one of three SWD-causing mutations (<i>Gabrg2</i>^{<i>tm1Spet(R43Q)</i>}, <i>Scn8a</i>^<i>8j</i> or <i>Gria4</i>^<i>spkw1</i>), demonstrated an antagonistic epistatic interaction between loci on mouse chromosomes 2 and 7 influencing SWD. These results implicate universal modifiers in the B6 background that mitigate SWD severity through a common pathway, independent of the causal mutation. In this study, we prioritized candidate modifiers in these interacting loci. Our approach integrated human genome-wide association results with gene interaction networks and mouse brain gene expression to prioritize candidate genes and pathways driving variation in SWD outcomes. We considered candidate genes that are functionally associated with human GGE risk genes and genes with evidence for coding or non-coding allele effects between the B6 and C3H backgrounds. Our analyses output a summary ranking of gene pairs, one gene from each locus, as candidates for explaining the epistatic interaction. Our top-ranking gene pairs implicate microtubule function, cytoskeletal stability and cell cycle regulation as novel hypotheses about the source of SWD variation across strain backgrounds, which could clarify underlying mechanisms driving differences in GGE severity in humans.</p>","PeriodicalId":50426,"journal":{"name":"Genes Brain and Behavior","volume":"23 2","pages":""},"PeriodicalIF":2.5,"publicationDate":"2024-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/gbb.12879","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140040737","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mutation of novel ethanol-responsive lncRNA Gm41261 impacts ethanol-related behavioral responses in mice","authors":"S. L. Plasil,&nbsp;S. P. Farris,&nbsp;Y. Blednov,&nbsp;R. D. Mayfield,&nbsp;R. A. Mangieri,&nbsp;U. J. Nwokeji,&nbsp;H. C. Aziz,&nbsp;P. S. Lambeth,&nbsp;R. A. Harris,&nbsp;G. E. Homanics","doi":"10.1111/gbb.12886","DOIUrl":"10.1111/gbb.12886","url":null,"abstract":"<p>Chronic alcohol exposure results in widespread dysregulation of gene expression that contributes to the pathogenesis of Alcohol Use Disorder (AUD). Long noncoding RNAs are key regulators of the transcriptome that we hypothesize coordinate alcohol-induced transcriptome dysregulation and contribute to AUD. Based on RNA-Sequencing data of human prefrontal cortex, basolateral amygdala and nucleus accumbens of AUD versus non-AUD brain, the human <i>LINC01265</i> and its predicted murine homolog <i>Gm41261</i> (i.e., TX2) were selected for functional interrogation. We tested the hypothesis that TX2 contributes to ethanol drinking and behavioral responses to ethanol. CRISPR/Cas9 mutagenesis was used to create a TX2 mutant mouse line in which 306 base-pairs were deleted from the locus. RNA analysis revealed that an abnormal TX2 transcript was produced at an unchanged level in mutant animals. Behaviorally, mutant mice had reduced ethanol, gaboxadol and zolpidem-induced loss of the righting response and reduced tolerance to ethanol in both sexes. In addition, a male-specific reduction in two-bottle choice every-other-day ethanol drinking was observed. Male TX2 mutants exhibited evidence of enhanced GABA release and altered GABA_A receptor subunit composition in neurons of the nucleus accumbens shell. In C57BL6/J mice, TX2 within the cortex was cytoplasmic and largely present in <i>Rbfox3</i>+ neurons and IBA1+ microglia, but not in <i>Olig2</i>+ oligodendrocytes or in the majority of GFAP+ astrocytes. These data support the hypothesis that TX2 mutagenesis and dysregulation impacts ethanol drinking behavior and ethanol-induced behavioral responses in mice, likely through alterations in the GABAergic system.</p>","PeriodicalId":50426,"journal":{"name":"Genes Brain and Behavior","volume":"23 1","pages":""},"PeriodicalIF":2.5,"publicationDate":"2024-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/gbb.12886","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139906786","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association of tameness and sociability but no sign of domestication syndrome in mice selectively bred for active tameness","authors":"Bharathi Venkatachalam,&nbsp;Bhim B. Biswa,&nbsp;Hiromichi Nagayama,&nbsp;Tsuyoshi Koide","doi":"10.1111/gbb.12887","DOIUrl":"10.1111/gbb.12887","url":null,"abstract":"<p>Domesticated animals have been developed by selecting desirable traits following the initial unconscious selection stage, and now exhibit phenotypes desired by humans. Tameness is a common behavioural trait found in all domesticated animals. At the same time, these domesticated animals exhibit a variety of morphological, behavioural, and physiological traits that differ from their wild counterparts of their ancestral species. These traits are collectively referred to as domestication syndrome. However, whether this phenomenon exists is debatable. Previously, selective breeding has been used to enhance active tameness, a motivation to interact with humans, in wild heterogeneous stock mice derived from eight wild inbred strains. In the current study, we used tame mice to study how selective breeding for active tameness affects behavioural and morphological traits. A series of behavioural and morphological analyses on mice showed an increased preference for social stimuli and a longer duration of engagement in non-aggressive behaviour. However, no differences were observed in exploratory or anxiety-related behaviours. Similarly, selection for tameness did not affect ultrasonic vocalisations in mice, and no changes were observed in known morphological traits associated with domestication syndrome. These results suggest that there may be a link between active tameness and sociability and provide insights into the relationship between tameness and other behaviours in the context of domestication.</p>","PeriodicalId":50426,"journal":{"name":"Genes Brain and Behavior","volume":"23 1","pages":""},"PeriodicalIF":2.5,"publicationDate":"2024-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/gbb.12887","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139906837","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Increased burden of rare protein-truncating variants in constrained, brain-specific and synaptic genes in extremely impulsively violent males with antisocial personality disorder","authors":"Dita Mušálková,&nbsp;Anna Přistoupilová,&nbsp;Ivana Jedličková,&nbsp;Hana Hartmannová,&nbsp;Helena Trešlová,&nbsp;Lenka Nosková,&nbsp;Kateřina Hodaňová,&nbsp;Petra Bittmanová,&nbsp;Viktor Stránecký,&nbsp;Václav Jiřička,&nbsp;Michaela Langmajerová,&nbsp;Marc Woodbury-Smith,&nbsp;Mehdi Zarrei,&nbsp;Brett Trost,&nbsp;Stephen W. Scherer,&nbsp;Anthony J. Bleyer,&nbsp;Jan Vevera,&nbsp;Stanislav Kmoch","doi":"10.1111/gbb.12882","DOIUrl":"10.1111/gbb.12882","url":null,"abstract":"<p>The genetic correlates of extreme impulsive violence are poorly understood, and there have been few studies that have characterized a large group of affected individuals both clinically and genetically. We performed whole exome sequencing (WES) in 290 males with the life-course-persistent, extremely impulsively violent form of antisocial personality disorder (APD) and analyzed the spectrum of rare protein-truncating variants (rPTVs). Comparisons were made with 314 male controls and publicly available genotype data. Functional annotation tools were used for biological interpretation. Participants were significantly more likely to harbor rPTVs in genes that are intolerant to loss-of-function variants (odds ratio [OR] 2.06; <i>p</i> &lt; 0.001), specifically expressed in brain (OR 2.80; <i>p</i> = 0.036) and enriched for those involved in neurotransmitter transport and synaptic processes. In 60 individuals (20%), we identified rPTVs that we classified as clinically relevant based on their clinical associations, biological function and gene expression patterns. Of these, 37 individuals harbored rPTVs in 23 genes that are associated with a monogenic neurological disorder, and 23 individuals harbored rPTVs in 20 genes reportedly intolerant to loss-of-function variants. The analysis presents evidence in support of a model where presence of either one or several private, functionally relevant mutations contribute significantly to individual risk of life-course-persistent APD and reveals multiple individuals who could be affected by clinically unrecognized neuropsychiatric Mendelian disease. Thus, Mendelian diseases and increased rPTV burden may represent important factors for the development of extremely impulsive violent life-course-persistent forms of APD irrespective of their clinical presentation.</p>","PeriodicalId":50426,"journal":{"name":"Genes Brain and Behavior","volume":"23 1","pages":""},"PeriodicalIF":2.5,"publicationDate":"2024-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/gbb.12882","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139742585","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neuropsychiatric disorders, chronotype and sleep: A narrative review of GWAS findings and the application of Mendelian randomization to investigate causal relationships","authors":"Shane Crinion,&nbsp;Derek W. Morris,&nbsp;Lorna M. Lopez","doi":"10.1111/gbb.12885","DOIUrl":"10.1111/gbb.12885","url":null,"abstract":"<p>Genome-wide association studies (GWAS) have been important for characterizing the genetic component and enhancing our understanding of the biological aetiology of both neuropsychiatric disorders and sleep-related phenotypes such as chronotype, which is our preference for morning or evening time. Mendelian randomization (MR) is a post-GWAS analysis that is used to infer causal relationships between potential risk factors and outcomes. MR uses genetic variants as instrumental variants for exposures to study the effect on outcomes. This review details the main results from GWAS of neuropsychiatric disorders and sleep-related phenotypes, and the application of MR to investigate their bidirectional relationship. The main results from MR studies of neuropsychiatric disorders and sleep-related phenotypes are summarized. These MR studies have identified 37 causal relationships between neuropsychiatric disorders and sleep-related phenotypes. MR studies identified evidence of a causal role for five neuropsychiatric disorders and symptoms (attention deficit hyperactivity disorder, bipolar disorder, depressive symptoms, major depressive disorder and schizophrenia) on sleep-related phenotypes and evidence of a causal role for five sleep-related phenotypes (daytime napping, insomnia, morning person, long sleep duration and sleep duration) on risk for neuropsychiatric disorders. These MR results show a bidirectional relationship between neuropsychiatric disorders and sleep-related phenotypes and identify potential risk factors for follow-up studies.</p>","PeriodicalId":50426,"journal":{"name":"Genes Brain and Behavior","volume":"23 1","pages":""},"PeriodicalIF":2.5,"publicationDate":"2024-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/gbb.12885","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139742586","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}