scholarly journals Transdiagnostic psychiatric disorder risk associated with early age of menarche: A latent modeling approach

2017 ◽  
Vol 79 ◽  
pp. 70-79 ◽  
Author(s):  
Jonathan M. Platt ◽  
Natalie L. Colich ◽  
Katie A. McLaughlin ◽  
Dahsan Gary ◽  
Katherine M. Keyes
Keyword(s):  
Psychiatric Disorder ◽  
Early Age ◽  
Modeling Approach ◽  
Latent Modeling ◽  
Age Of Menarche ◽  
Disorder Risk

scholarly journals Genome-wide landscape of RNA-binding protein target site dysregulation reveals a major impact on psychiatric disorder risk

2021 ◽  
Vol 53 (2) ◽  
pp. 166-173
Author(s):  
Christopher Y. Park ◽  
Jian Zhou ◽  
Aaron K. Wong ◽  
Kathleen M. Chen ◽  
Chandra L. Theesfeld ◽  
...  
Keyword(s):  
Psychiatric Disorder ◽  
Rna Binding ◽  
Binding Protein ◽  
Rna Binding Protein ◽  
Target Site ◽  
Protein Target ◽  
Genome Wide ◽  
Disorder Risk

Gender Differences in the Link Between Cyberbullying and Parental Supervision Trajectories

2020 ◽  
Vol 66 (13-14) ◽  
pp. 1914-1936
Author(s):  
Hyojong Song ◽  
Yeungjeom Lee ◽  
Jihoon Kim
Keyword(s):  
Gender Differences ◽  
Parental Supervision ◽  
Early Age ◽  
Trajectory Modeling ◽  
Longitudinal Sample ◽  
South Korean ◽  
Modeling Approach ◽  
Korean Youth ◽  
And Gender ◽  
Latent Group

This study aims to explore joint trajectories of parental supervision and cyberbullying for boys and girls, respectively. Drawing on a longitudinal sample of South Korean youth, we employ a latent group-based trajectory modeling approach to examine overlapping patterns of parental supervision and cyberbullying trajectories, and gender differences in the bivariate overlap. We found that boys with higher levels of parental supervision were more likely to be in the Noninvolved cyberbullying group, whereas girls with the highest level of parental supervision tended to engage in cyberbullying at an early age but soon desisted from it after the initial involvement. Results suggest that effects of parental supervision on cyberbullying may vary across gender.

29GENETIC ASSOCIATIONS BETWEEN PSYCHIATRIC DISORDER RISK AND PHENOTYPIC FACTORS IN THE UK BIOBANK

2019 ◽  
Vol 29 ◽  
pp. S1082-S1083
Author(s):  
Caitlin Carey ◽  
Rebecca Shafee ◽  
Raymond Walters ◽  
Duncan Palmer ◽  
Liam Abbott ◽  
...  
Keyword(s):  
Psychiatric Disorder ◽  
Uk Biobank ◽  
The Uk ◽  
Disorder Risk

scholarly journals Feasibility and application of polygenic score analysis to the morphology of human induced pluripotent stem cells

2020 ◽  
Author(s):  
Jonathan R. I. Coleman
Keyword(s):  
Stem Cells ◽  
Psychiatric Disorder ◽  
Induced Pluripotent Stem Cells ◽  
Pluripotent Stem Cells ◽  
Complex Traits ◽  
European Ancestry ◽  
Genome Wide Association Studies ◽  
Polygenic Score ◽  
Induced Pluripotent ◽  
Disorder Risk

AbstractGenome-wide association studies have identified thousands of significant associations between genetic variants and complex traits. Inferring biological insights from these associations has been challenging. One approach attempted has been to examine the effects of individual variants in cellular models. Here, I demonstrate the feasibility of examining the aggregate effect of many variants on cellular phenotypes. I examine the effects of polygenic scores for cross-psychiatric disorder risk, schizophrenia, body mass index and height on cellular morphology, using 1.5 million induced pluripotent stem cells (iPSC) from 60 European-ancestry donors from the Human iPSC Initiative dataset. I show that measuring multiple cells per donor provides sufficient power for polygenic score analyses, and that cross-psychiatric disorder risk is associated with cell area (p = 0.004). Combined with emerging methods of high-throughput iPSC phenotyping, cellular polygenic scoring is a promising method for understanding potential biological effects of the polygenic component of complex traits.

scholarly journals The neurobiology of BRD1 implicates sex-biased dysregulation of nuclear receptor signaling in mental disorders

2018 ◽  
Author(s):  
Anto P. Rajkumar ◽  
Per Qvist ◽  
Sanne H. Larsen ◽  
Ross Lazarus ◽  
Jonatan Pallesen ◽  
...  
Keyword(s):  
Psychiatric Disorder ◽  
Nuclear Receptors ◽  
Nuclear Receptor ◽  
Glucocorticoid Receptors ◽  
Target Genes ◽  
Global Gene Expression ◽  
Adult Brain ◽  
Gene Sets ◽  
Disorder Risk

AbstractThe schizophrenia and bipolar disorder associated gene, BRD1, encodes a scaffold protein that in complex with epigenetic modifiers regulate gene sets enriched for psychiatric disorder risk. Preclinical evidence from male Brd1+/− mice has previously implicated BRD1 with phenotypes of translational relevance to schizophrenia. Here we describe the phenotype of female Brd1+/− mice and report attenuated dendritic architecture and monoaminergic dysregulation accompanied by sex-specific changes in affective behaviors. In accordance, global gene expression profiling reveals regional dysregulation of gene sets enriched with major depressive disorder and schizophrenia risk in female and male Brd1+/− mice, respectively. Independent of sex, however, differentially expressed genes cluster in common functional pathways associated with psychiatric disorders, including mitochondrial dysfunction and oxidative phosphorylation as well as G-protein coupled-, and nuclear receptor mediated signaling. Accordingly, we provide in vitro evidence that BRD1 modulates the transcriptional drive of a subset of nuclear receptors (e.g. the vitamin D and glucocorticoid receptors). Moreover, we demonstrate enrichment of psychiatric disorder risk in the target genes of nuclear receptors, sex-biased expression of several nuclear receptor genes in the adult brain of Brd1+/− mice, and that sex-biased genes in general are enriched with nuclear receptor genes particularly at the earliest developmental stage of the human brain. Overall, our data suggests that the spatio-temporal interaction between BRD1 and subsets of nuclear receptors in the brain is sex-biased and that hampered BRD1 mediated regulation of target genes governed by certain nuclear receptors may significantly contribute to sex differences in psychopathology.

scholarly journals Genome-wide landscape of RNA-binding protein dysregulation reveals a major impact on psychiatric disorder risk

2020 ◽  
Author(s):  
Christopher Y. Park ◽  
Jian Zhou ◽  
Aaron K. Wong ◽  
Kathleen M. Chen ◽  
Chandra L. Theesfeld ◽  
...  
Keyword(s):  
Psychiatric Disorder ◽  
Psychiatric Disorders ◽  
Large Scale ◽  
Complex Disease ◽  
Rna Binding ◽  
Rna Binding Proteins ◽  
Full Range ◽  
Coding Region ◽  
Genome Wide ◽  
Disorder Risk

AbstractDespite the strong genetic basis of psychiatric disorders, the molecular origins of these diseases are still largely unmapped. RNA-binding proteins (RBPs) are responsible for most post-transcriptional regulation, from splicing to translational to localization. RBPs thus act as key gatekeepers of cellular homeostasis, especially in the brain. Here, we leverage a deep learning approach to interrogate variant effects genome-wide, and discover that the dysregulation of RBP target sites is a principal contributor to psychiatric disorder risk. We show that specific modes of RBP regulation are genetically linked to the heritability of psychiatric disorders, and demonstrate that diverse RBP regulatory functions are reflected in distinct genome-wide negative selection signatures. Notably, RBP dysregulation has a stronger impact on psychiatric disorders than common coding region variants and explains heritability not currently captured by large-scale molecular QTL studies (expression QTLs and splicing QTLs). We share genome-wide profiles of RBP target site dysregulation, which we used to identify DDHD2 as a candidate schizophrenia risk gene, in a public web server. This resource provides a novel analytical framework to connect the full range of RNA regulation to complex disease.

scholarly journals Age at Onset of Menarche and Puberty of Girls in Aydin Region and the Factors Affecting Them

2021 ◽  
Author(s):  
Ebru Ataş Aslan
Keyword(s):  
Rural Areas ◽  
Age At Onset ◽  
Female Students ◽  
Age At Menarche ◽  
Early Age ◽  
Onset Age ◽  
Factors Affecting ◽  
The Mean ◽  
Experienced Physician ◽  
Age Of Menarche

INTRODUCTION: In this study, we aimed to determine the range of mean age at onset of menarche (AOM) and puberty (AOP) of girls living in Aydin province and to determine the factors affecting the onset age of menarche. METHODS: A total of 1891 girls aged between 8 and 16 years attending primary, secondary and high schools in Aydin province were planned to be included in the study. A questionnaire that was prepared in line with the literature was delivered to the parents in a closed envelope. The subjects who accepted to participate in the study were examined by an experienced physician by measuring height and weight and pubertal status was defined according to Tanner scale. BMI values were calculated. RESULTS: In total, 1520 female students were accepted to the study with the permission of their families. The mean AOM of participants was 12.11±1.32 years. The mean AOM was 13.12±1.46 years for their mothers, and 12.73±1.25 years for their sisters. June was the month that menarche occurred most frequently. We observed that the children living in rural areas had an earlier age of menarche. The mean age at onset of puberty was 9.71±1.46 years. DISCUSSION AND CONCLUSION: Our study is important in terms of being the first study conducted in Aydin province that determined the mean AOM and AOP of girls aged between 8 and 16. In our study, we showed that the age of menarche shifted to an early age, while the age of puberty did not shift. The age at onset of menarche and puberty were similar to the results obtained in other studies conducted in neighboring regions. We believe that larger scale studies may contribute to assess the actual mean age at menarche of girls living in Turkey.

scholarly journals The impact of telomere shortening on human hippocampal neurogenesis: Implications for cognitive function and psychiatric disorder risk

2020 ◽  
Author(s):  
Alish B. Palmos ◽  
Rodrigo R. R. Duarte ◽  
Demelza M. Smeeth ◽  
Erin C. Hedges ◽  
Douglas F. Nixon ◽  
...  
Keyword(s):  
Cognitive Function ◽  
Psychiatric Disorder ◽  
Progenitor Cells ◽  
Hippocampal Neurogenesis ◽  
Gene Set Enrichment Analysis ◽  
Telomere Maintenance ◽  
Proliferative Capacity ◽  
Telomere Shortening ◽  
Age Related ◽  
Disorder Risk

AbstractTelomere shortening is one hallmark of cell ageing that can limit the proliferative capacity of cell populations and increase risk for age-related disease. It has been hypothesized that short telomeres, and subsequently a limited proliferative capacity of hippocampal progenitor cells, could contribute to smaller hippocampal volumes and impaired cognition, amongst psychiatric disorder patients. The current study employed a systematic, multidisciplinary approach which aimed to model the effects of telomere shortening on human hippocampal neurogenesis, and to explore its relationship with cognition and psychiatric disorder risk. We modelled telomere shortening in human hippocampal progenitor cells in vitro using a serial passaging protocol that mimics the end-replication problem. Aged progenitors demonstrated shorter telomeres (p<0.05), and reduced rates of cell proliferation, as marked by bromodeoxyuridine staining (p<0.001), with no changes in the ability of cells to differentiate into neurons or glia. RNA-sequencing and gene set enrichment analysis revealed an effect of cell ageing on gene networks related to neurogenesis, telomere maintenance, cell senescence and cytokine production. Downregulated transcripts showed a significant overlap with genes regulating cognitive function and risk for schizophrenia and bipolar disorder. Collectively, our results suggest that reductions in adult hippocampal neurogenesis, caused by telomere shortening, could represent a cellular mechanism contributing to age-related cognitive impairment and psychiatric disorder risk.

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