The Experts below are selected from a list of 7554 Experts worldwide ranked by ideXlab platform
Alan S Brown - One of the best experts on this subject based on the ideXlab platform.
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epidemiologic studies of exposure to prenatal infection and risk of Schizophrenia and autism
2012Co-Authors: Alan S BrownAbstract:In this review, we provide a synopsis of work on the epidemiologic evidence for prenatal infection in the Etiology of Schizophrenia and autism. In birth cohort studies conducted by our group and others, in utero exposure to infectious agents, prospectively obtained after biomarker assays of archived maternal sera and by obstetric records was related to an increased risk of Schizophrenia. Thus far, it has been demonstrated that prenatal exposure to influenza, increased toxoplasma antibody, genital-reproductive infections, rubella, and other pathogens are associated with Schizophrenia. Anomalies of the immune system, including enhanced maternal cytokine levels, are also related to Schizophrenia. Some evidence also suggests that maternal infection and immune dysfunction may be associated with autism. Although replication is required, these findings suggest that public health interventions targeting infectious exposures have the potential for preventing cases of Schizophrenia and autism. Moreover, this work has stimulated translational research on the neurobiological and genetic determinants of these conditions.
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prenatal infection and Schizophrenia a review of epidemiologic and translational studies
2010Co-Authors: Alan S Brown, Elena J DerkitsAbstract:AbstractAn emerging literature from epidemiologic, clinical, and preclinical investigations has provided evidence that gestational exposure to infection contributes to the Etiology of Schizophrenia. In recent years, these studies have moved from ecologic designs, which ascertain infection based on epidemics in populations, to investigations that have capitalized on reliable biomarkers in individual pregnancies. These studies have documented specific candidate infections that appear to be associated with an elevated risk of Schizophrenia. Animal models of maternal immune activation inspired by this work have revealed intriguing findings indicating behavioral, neurochemical, and neurophysiologic abnormalities consistent with observations in Schizophrenia. In parallel studies in humans and animals, investigators are working to uncover the cellular and molecular mechanisms by which in utero exposure to infection contributes to Schizophrenia risk. In this review, the authors discuss and critically evaluate the...
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serologic evidence of prenatal influenza in the Etiology of Schizophrenia
2005Co-Authors: Alan S Brown, Richard Jed Wyatt, Melissa D Begg, Stefan Gravenstein, Catherine Schaefer, Michaeline Bresnahan, Vicki P Babulas, Ezra SusserAbstract:Context: Some, but not all, previous studies suggest that prenatal influenza exposure increases the risk of Schizophrenia. These studies used dates of influenza epidemics and maternal recall of infection to define influenza exposure, suggesting that discrepant findings may have resulted from exposure misclassification. Objective: To examine whether serologically documented prenatal exposure to influenza increases the risk of Schizophrenia. Design: Nested case-control study of a large birth cohort, born from 1959 through 1966, and followed up for psychiatric disorders 30 to 38 years later. Setting: Population-based birth cohort. Participants: Cases were 64 birth cohort members diagnosed as having Schizophrenia spectrum disorders (mostly Schizophrenia and schizoaffective disorder). Controls were 125 members of the birth cohort, had not been diagnosed as having a Schizophrenia spectrum or major affective disorder, and were matched to cases on date of birth, sex, length of time in the cohort, and availability of maternal serum. Main Outcome Measures: Archived maternal serum was assayed for influenza antibody in pregnancies giving rise to offspring with Schizophrenia and matched control offspring. Results: The risk of Schizophrenia was increased 7-fold for influenza exposure during the first trimester. There was no increased risk of Schizophrenia with influenza during the second or third trimester. With the use of a broader gestationalperiodofinfluenzaexposure—earlytomidpregnancy— the risk of Schizophrenia was increased 3-fold. The findings persisted after adjustment for potential confounders. Conclusions: These findings represent the first serologic evidence that prenatal influenza plays a role in Schizophrenia. If confirmed, the results may have implications for the prevention of Schizophrenia and for unraveling pathogenic mechanisms of the disorder. Arch Gen Psychiatry. 2004;61:774-780
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serologic evidence of prenatal influenza in the Etiology of Schizophrenia
2004Co-Authors: Alan S Brown, Richard Jed Wyatt, Melissa D Begg, Stefan Gravenstein, Catherine Schaefer, Michaeline Bresnahan, Vicki P Babulas, Ezra SusserAbstract:Context Some, but not all, previous studies suggest that prenatal influenza exposure increases the risk of Schizophrenia. These studies used dates of influenza epidemics and maternal recall of infection to define influenza exposure, suggesting that discrepant findings may have resulted from exposure misclassification. Objective To examine whether serologically documented prenatal exposure to influenza increases the risk of Schizophrenia. Design Nested case-control study of a large birth cohort, born from 1959 through 1966, and followed up for psychiatric disorders 30 to 38 years later. Setting Population-based birth cohort. Participants Cases were 64 birth cohort members diagnosed as having Schizophrenia spectrum disorders (mostly Schizophrenia and schizoaffective disorder). Controls were 125 members of the birth cohort, had not been diagnosed as having a Schizophrenia spectrum or major affective disorder, and were matched to cases on date of birth, sex, length of time in the cohort, and availability of maternal serum. Main Outcome Measures Archived maternal serum was assayed for influenza antibody in pregnancies giving rise to offspring with Schizophrenia and matched control offspring. Results The risk of Schizophrenia was increased 7-fold for influenza exposure during the first trimester. There was no increased risk of Schizophrenia with influenza during the second or third trimester. With the use of a broader gestational period of influenza exposure—early to midpregnancy—the risk of Schizophrenia was increased 3-fold. The findings persisted after adjustment for potential confounders. Conclusions These findings represent the first serologic evidence that prenatal influenza plays a role in Schizophrenia. If confirmed, the results may have implications for the prevention of Schizophrenia and for unraveling pathogenic mechanisms of the disorder.
Franck Schurhoff - One of the best experts on this subject based on the ideXlab platform.
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Schizophrenia developmental variability interacts with risk factors to cause the disorder nonspecific variability enhancing factors combine with specific risk factors to cause Schizophrenia
2020Co-Authors: Andrei Szoke, Baptiste Pignon, Sarah Boster, Stephane Jamain, Franck SchurhoffAbstract:A new etiological model is proposed for Schizophrenia that combines variability-enhancing nonspecific factors acting during development with more specific risk factors. This model is better suited than the current etiological models of Schizophrenia, based on the risk factors paradigm, for predicting and/or explaining several important findings about Schizophrenia: high co-morbidity rates, low specificity of many risk factors, and persistence in the population of the associated genetic polymorphisms. Compared with similar models, e.g., de-canalization, common psychopathology factor, sexual-selection, or differential sensitivity to the environment, this proposal is more general and integrative. Recently developed research methods have proven the existence of genetic and environmental factors that enhance developmental variability. Applying such methods to newly collected or already available data can allow for testing the hypotheses upon which this model is built. If validated, this model may change the understanding of the Etiology of Schizophrenia, the research models, and preventionbrk paradigms.
Ezra Susser - One of the best experts on this subject based on the ideXlab platform.
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serologic evidence of prenatal influenza in the Etiology of Schizophrenia
2005Co-Authors: Alan S Brown, Richard Jed Wyatt, Melissa D Begg, Stefan Gravenstein, Catherine Schaefer, Michaeline Bresnahan, Vicki P Babulas, Ezra SusserAbstract:Context: Some, but not all, previous studies suggest that prenatal influenza exposure increases the risk of Schizophrenia. These studies used dates of influenza epidemics and maternal recall of infection to define influenza exposure, suggesting that discrepant findings may have resulted from exposure misclassification. Objective: To examine whether serologically documented prenatal exposure to influenza increases the risk of Schizophrenia. Design: Nested case-control study of a large birth cohort, born from 1959 through 1966, and followed up for psychiatric disorders 30 to 38 years later. Setting: Population-based birth cohort. Participants: Cases were 64 birth cohort members diagnosed as having Schizophrenia spectrum disorders (mostly Schizophrenia and schizoaffective disorder). Controls were 125 members of the birth cohort, had not been diagnosed as having a Schizophrenia spectrum or major affective disorder, and were matched to cases on date of birth, sex, length of time in the cohort, and availability of maternal serum. Main Outcome Measures: Archived maternal serum was assayed for influenza antibody in pregnancies giving rise to offspring with Schizophrenia and matched control offspring. Results: The risk of Schizophrenia was increased 7-fold for influenza exposure during the first trimester. There was no increased risk of Schizophrenia with influenza during the second or third trimester. With the use of a broader gestationalperiodofinfluenzaexposure—earlytomidpregnancy— the risk of Schizophrenia was increased 3-fold. The findings persisted after adjustment for potential confounders. Conclusions: These findings represent the first serologic evidence that prenatal influenza plays a role in Schizophrenia. If confirmed, the results may have implications for the prevention of Schizophrenia and for unraveling pathogenic mechanisms of the disorder. Arch Gen Psychiatry. 2004;61:774-780
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serologic evidence of prenatal influenza in the Etiology of Schizophrenia
2004Co-Authors: Alan S Brown, Richard Jed Wyatt, Melissa D Begg, Stefan Gravenstein, Catherine Schaefer, Michaeline Bresnahan, Vicki P Babulas, Ezra SusserAbstract:Context Some, but not all, previous studies suggest that prenatal influenza exposure increases the risk of Schizophrenia. These studies used dates of influenza epidemics and maternal recall of infection to define influenza exposure, suggesting that discrepant findings may have resulted from exposure misclassification. Objective To examine whether serologically documented prenatal exposure to influenza increases the risk of Schizophrenia. Design Nested case-control study of a large birth cohort, born from 1959 through 1966, and followed up for psychiatric disorders 30 to 38 years later. Setting Population-based birth cohort. Participants Cases were 64 birth cohort members diagnosed as having Schizophrenia spectrum disorders (mostly Schizophrenia and schizoaffective disorder). Controls were 125 members of the birth cohort, had not been diagnosed as having a Schizophrenia spectrum or major affective disorder, and were matched to cases on date of birth, sex, length of time in the cohort, and availability of maternal serum. Main Outcome Measures Archived maternal serum was assayed for influenza antibody in pregnancies giving rise to offspring with Schizophrenia and matched control offspring. Results The risk of Schizophrenia was increased 7-fold for influenza exposure during the first trimester. There was no increased risk of Schizophrenia with influenza during the second or third trimester. With the use of a broader gestational period of influenza exposure—early to midpregnancy—the risk of Schizophrenia was increased 3-fold. The findings persisted after adjustment for potential confounders. Conclusions These findings represent the first serologic evidence that prenatal influenza plays a role in Schizophrenia. If confirmed, the results may have implications for the prevention of Schizophrenia and for unraveling pathogenic mechanisms of the disorder.
Stephane Jamain - One of the best experts on this subject based on the ideXlab platform.
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Schizophrenia developmental variability interacts with risk factors to cause the disorder nonspecific variability enhancing factors combine with specific risk factors to cause Schizophrenia
2020Co-Authors: Andrei Szoke, Baptiste Pignon, Sarah Boster, Stephane Jamain, Franck SchurhoffAbstract:A new etiological model is proposed for Schizophrenia that combines variability-enhancing nonspecific factors acting during development with more specific risk factors. This model is better suited than the current etiological models of Schizophrenia, based on the risk factors paradigm, for predicting and/or explaining several important findings about Schizophrenia: high co-morbidity rates, low specificity of many risk factors, and persistence in the population of the associated genetic polymorphisms. Compared with similar models, e.g., de-canalization, common psychopathology factor, sexual-selection, or differential sensitivity to the environment, this proposal is more general and integrative. Recently developed research methods have proven the existence of genetic and environmental factors that enhance developmental variability. Applying such methods to newly collected or already available data can allow for testing the hypotheses upon which this model is built. If validated, this model may change the understanding of the Etiology of Schizophrenia, the research models, and preventionbrk paradigms.
Jonathan Weitz - One of the best experts on this subject based on the ideXlab platform.
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gene expression in patient derived neural progenitors implicates wnt5a signaling in the Etiology of Schizophrenia
2020Co-Authors: Oleg V Evgrafov, Chris Armoskus, Bozena Wrobel, Valeria N Spitsyna, Tade Souaiaia, Jennifer Herstein, Christopher Walker, Joseph D Nguyen, Adrian Camarena, Jonathan WeitzAbstract:Abstract Background Genome-wide association studies of Schizophrenia have demonstrated that variations in noncoding regions are responsible for most of the common variation heritability of the disease. It is hypothesized that these risk variants alter gene expression. Therefore, studying alterations in gene expression in Schizophrenia may provide a direct approach to understanding the Etiology of the disease. In this study we use cultured neural progenitor cells derived from olfactory neuroepithelium (CNON cells) as a genetically unaltered cellular model to elucidate the neurodevelopmental aspects of Schizophrenia. Methods We performed a gene expression study using RNA sequencing of CNON cells from 111 control subjects and 144 individuals with Schizophrenia. Differentially expressed genes were identified with DESeq2 software, using covariates to correct for sex, age, library batches, and 1 surrogate variable component. Results A total of 80 genes were differentially expressed (false discovery rate Conclusions CNON cells are a good model of the neurodevelopmental aspects of Schizophrenia and can be used to elucidate the Etiology of the disorder.