184 recherche sur le mot-clé 'environment'

Long-term spatial tracking of cells affected by environmental insults / Shahid MOHAMMAD in Journal of Neurodevelopmental Disorders, 12 (2020)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 12 (2020) Titre : Long-term spatial tracking of cells affected by environmental insults Type de document : texte imprimé Auteurs : Shahid MOHAMMAD, Auteur ; Stephen J. PAGE, Auteur ; Toru SASAKI, Auteur ; Nicholas AYVAZIAN, Auteur ; Pasko RAKIC, Auteur ; Yuka Imamura KAWASAWA, Auteur ; Kazue HASHIMOTO-TORII, Auteur ; Masaaki TORII, Auteur Langues : Anglais (eng) Mots-clés : Animals  Brain/embryology/growth & development  Environment  Female  Mice  Mice, Transgenic  Neurons  Pregnancy  Prenatal Exposure Delayed Effects  Brain development  Environmental stress  Heat shock signaling  Lineage tracing  Reporter Index. décimale : PER Périodiques Résumé : BACKGROUND: Harsh environments surrounding fetuses and children can induce cellular damage in the developing brain, increasing the risk of intellectual disability and other neurodevelopmental disorders such as schizophrenia. However, the mechanisms by which early damage leads to disease manifestation in later life remain largely unknown. Previously, we demonstrated that the activation of heat shock (HS) signaling can be utilized as a unique reporter to label the cells that undergo specific molecular/cellular changes upon exposure to environmental insults throughout the body. Since the activation of HS signaling is an acute and transient event, this approach was not intended for long-term tracing of affected cells after the activation has diminished. In the present study, we generated new reporter transgenic mouse lines as a novel tool to achieve systemic and long-term tracking of affected cells and their progeny. METHODS: The reporter transgenic mouse system was designed so that the activation of HS signaling through HS response element (HSE) drives flippase (FLPo)-flippase recognition target (FRT) recombination-mediated permanent expression of the red fluorescent protein (RFP), tdTomato. With a priority on consistent and efficient assessment of the reporter system, we focused on intraperitoneal (i.p.) injection models of high-dose, short prenatal exposure to alcohol (ethanol) and sodium arsenite (ethanol at 4.0 g/kg/day and sodium arsenite at 5.0 mg/kg/day, at embryonic day (E) 12 and 13). Long-term reporter expression was examined in the brain of reporter mice that were prenatally exposed to these insults. Electrophysiological properties were compared between RFP(+) and RFP(-) cortical neurons in animals prenatally exposed to arsenite. RESULTS: We detected RFP(+) neurons and glia in the brains of postnatal mice that had been prenatally exposed to alcohol or sodium arsenite. In animals prenatally exposed to sodium arsenite, we also detected reduced excitability in RFP(+) cortical neurons. CONCLUSION: The reporter transgenic mice allowed us to trace the cells that once responded to prenatal environmental stress and the progeny derived from these cells long after the exposure in postnatal animals. Tracing of these cells indicates that the impact of prenatal exposure on neural progenitor cells can lead to functional abnormalities in their progeny cells in the postnatal brain. Further studies using more clinically relevant exposure models are warranted to explore this mechanism. En ligne : https://dx.doi.org/10.1186/s11689-020-09339-w Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=573 [article] Long-term spatial tracking of cells affected by environmental insults [texte imprimé] / Shahid MOHAMMAD, Auteur ; Stephen J. PAGE, Auteur ; Toru SASAKI, Auteur ; Nicholas AYVAZIAN, Auteur ; Pasko RAKIC, Auteur ; Yuka Imamura KAWASAWA, Auteur ; Kazue HASHIMOTO-TORII, Auteur ; Masaaki TORII, Auteur. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 12 (2020) Mots-clés : Animals  Brain/embryology/growth & development  Environment  Female  Mice  Mice, Transgenic  Neurons  Pregnancy  Prenatal Exposure Delayed Effects  Brain development  Environmental stress  Heat shock signaling  Lineage tracing  Reporter Index. décimale : PER Périodiques Résumé : BACKGROUND: Harsh environments surrounding fetuses and children can induce cellular damage in the developing brain, increasing the risk of intellectual disability and other neurodevelopmental disorders such as schizophrenia. However, the mechanisms by which early damage leads to disease manifestation in later life remain largely unknown. Previously, we demonstrated that the activation of heat shock (HS) signaling can be utilized as a unique reporter to label the cells that undergo specific molecular/cellular changes upon exposure to environmental insults throughout the body. Since the activation of HS signaling is an acute and transient event, this approach was not intended for long-term tracing of affected cells after the activation has diminished. In the present study, we generated new reporter transgenic mouse lines as a novel tool to achieve systemic and long-term tracking of affected cells and their progeny. METHODS: The reporter transgenic mouse system was designed so that the activation of HS signaling through HS response element (HSE) drives flippase (FLPo)-flippase recognition target (FRT) recombination-mediated permanent expression of the red fluorescent protein (RFP), tdTomato. With a priority on consistent and efficient assessment of the reporter system, we focused on intraperitoneal (i.p.) injection models of high-dose, short prenatal exposure to alcohol (ethanol) and sodium arsenite (ethanol at 4.0 g/kg/day and sodium arsenite at 5.0 mg/kg/day, at embryonic day (E) 12 and 13). Long-term reporter expression was examined in the brain of reporter mice that were prenatally exposed to these insults. Electrophysiological properties were compared between RFP(+) and RFP(-) cortical neurons in animals prenatally exposed to arsenite. RESULTS: We detected RFP(+) neurons and glia in the brains of postnatal mice that had been prenatally exposed to alcohol or sodium arsenite. In animals prenatally exposed to sodium arsenite, we also detected reduced excitability in RFP(+) cortical neurons. CONCLUSION: The reporter transgenic mice allowed us to trace the cells that once responded to prenatal environmental stress and the progeny derived from these cells long after the exposure in postnatal animals. Tracing of these cells indicates that the impact of prenatal exposure on neural progenitor cells can lead to functional abnormalities in their progeny cells in the postnatal brain. Further studies using more clinically relevant exposure models are warranted to explore this mechanism. En ligne : https://dx.doi.org/10.1186/s11689-020-09339-w Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=573

Research Review: How to interpret associations between polygenic scores, environmental risks, and phenotypes / Jean-Baptiste PINGAULT in Journal of Child Psychology and Psychiatry, 63-10 (October 2022)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 63-10 (October 2022) . - p.1125-1139 Titre : Research Review: How to interpret associations between polygenic scores, environmental risks, and phenotypes Type de document : texte imprimé Auteurs : Jean-Baptiste PINGAULT, Auteur ; Andrea G. ALLEGRINI, Auteur ; Tracy ODIGIE, Auteur ; Leonard FRACH, Auteur ; Jessie R. BALDWIN, Auteur ; Frühling V. RIJSDIJK, Auteur ; Frank DUDBRIDGE, Auteur Année de publication : 2022 Article en page(s) : p.1125-1139 Langues : Anglais (eng) Mots-clés : Cohort Studies  Environmental Exposure/adverse effects  Genetic Predisposition to Disease  Genome-Wide Association Study  Humans  Midazolam  Multifactorial Inheritance  Phenotype  Polygenic scores  biases  environment  epidemiology  phenotypes Index. décimale : PER Périodiques Résumé : BACKGROUND: Genetic influences are ubiquitous as virtually all phenotypes and most exposures typically classified as environmental have been found to be heritable. A polygenic score summarises the associations between millions of genetic variants and an outcome in a single value for each individual. Ever lowering costs have enabled the genotyping of many samples relevant to child psychology and psychiatry research, including cohort studies, leading to the proliferation of polygenic score studies. It is tempting to assume that associations detected between polygenic scores and phenotypes in those studies only reflect genetic effects. However, such associations can reflect many pathways (e.g. via environmental mediation) and biases. METHODS: Here, we provide a comprehensive overview of the many reasons why associations between polygenic scores, environmental exposures, and phenotypes exist. We include formal representations of common analyses in polygenic score studies using structural equation modelling. We derive biases, provide illustrative empirical examples and, when possible, mention steps that can be taken to alleviate those biases. RESULTS: Structural equation models and derivations show the many complexities arising from jointly modelling polygenic scores with environmental exposures and phenotypes. Counter-intuitive examples include that: (a) associations between polygenic scores and phenotypes may exist even in the absence of direct genetic effects; (b) associations between child polygenic scores and environmental exposures can exist in the absence of evocative/active gene-environment correlations; and (c) adjusting an exposure-outcome association for a polygenic score can increase rather than decrease bias. CONCLUSIONS: Strikingly, using polygenic scores may, in some cases, lead to more bias than not using them. Appropriately conducting and interpreting polygenic score studies thus requires researchers in child psychology and psychiatry and beyond to be versed in both epidemiological and genetic methods or build on interdisciplinary collaborations. En ligne : http://dx.doi.org/10.1111/jcpp.13607 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=486 [article] Research Review: How to interpret associations between polygenic scores, environmental risks, and phenotypes [texte imprimé] / Jean-Baptiste PINGAULT, Auteur ; Andrea G. ALLEGRINI, Auteur ; Tracy ODIGIE, Auteur ; Leonard FRACH, Auteur ; Jessie R. BALDWIN, Auteur ; Frühling V. RIJSDIJK, Auteur ; Frank DUDBRIDGE, Auteur . - 2022 . - p.1125-1139. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 63-10 (October 2022) . - p.1125-1139 Mots-clés : Cohort Studies  Environmental Exposure/adverse effects  Genetic Predisposition to Disease  Genome-Wide Association Study  Humans  Midazolam  Multifactorial Inheritance  Phenotype  Polygenic scores  biases  environment  epidemiology  phenotypes Index. décimale : PER Périodiques Résumé : BACKGROUND: Genetic influences are ubiquitous as virtually all phenotypes and most exposures typically classified as environmental have been found to be heritable. A polygenic score summarises the associations between millions of genetic variants and an outcome in a single value for each individual. Ever lowering costs have enabled the genotyping of many samples relevant to child psychology and psychiatry research, including cohort studies, leading to the proliferation of polygenic score studies. It is tempting to assume that associations detected between polygenic scores and phenotypes in those studies only reflect genetic effects. However, such associations can reflect many pathways (e.g. via environmental mediation) and biases. METHODS: Here, we provide a comprehensive overview of the many reasons why associations between polygenic scores, environmental exposures, and phenotypes exist. We include formal representations of common analyses in polygenic score studies using structural equation modelling. We derive biases, provide illustrative empirical examples and, when possible, mention steps that can be taken to alleviate those biases. RESULTS: Structural equation models and derivations show the many complexities arising from jointly modelling polygenic scores with environmental exposures and phenotypes. Counter-intuitive examples include that: (a) associations between polygenic scores and phenotypes may exist even in the absence of direct genetic effects; (b) associations between child polygenic scores and environmental exposures can exist in the absence of evocative/active gene-environment correlations; and (c) adjusting an exposure-outcome association for a polygenic score can increase rather than decrease bias. CONCLUSIONS: Strikingly, using polygenic scores may, in some cases, lead to more bias than not using them. Appropriately conducting and interpreting polygenic score studies thus requires researchers in child psychology and psychiatry and beyond to be versed in both epidemiological and genetic methods or build on interdisciplinary collaborations. En ligne : http://dx.doi.org/10.1111/jcpp.13607 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=486

Annual Research Review: The role of the environment in the developmental psychopathology of autism spectrum condition / William MANDY in Journal of Child Psychology and Psychiatry, 57-3 (March 2016)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 57-3 (March 2016) . - p.271-292 Titre : Annual Research Review: The role of the environment in the developmental psychopathology of autism spectrum condition Type de document : texte imprimé Auteurs : William MANDY, Auteur ; Meng-Chuan LAI, Auteur Article en page(s) : p.271-292 Langues : Anglais (eng) Mots-clés : Autism spectrum condition  autism spectrum disorder  autism  Asperger's syndrome  genetics  environment  developmental psychopathology Index. décimale : PER Périodiques Résumé : Background Although autism spectrum condition (ASC) is strongly genetic in origin, accumulating evidence points to the critical roles of various environmental influences on its emergence and subsequent developmental course. Methods A developmental psychopathology framework was used to synthesise literature on environmental factors associated with the onset and course of ASC (based on a systematic search of the literature using PubMed, PsychInfo and Google Scholar databases). Particular emphasis was placed on gene–environment interplay, including gene–environment interaction (G × E) and gene–environment correlation (rGE). Results Before conception, advanced paternal and maternal ages may independently enhance offspring risk for ASC. Exogenous prenatal risks are evident (e.g. valproate and toxic chemicals) or possible (e.g. selective serotonin reuptake inhibitors), and processes endogenous to the materno-foeto-placental unit (e.g. maternal diabetes, enhanced steroidogenic activities and maternal immune activation) likely heighten offspring vulnerability to ASC. Folate intake is a prenatal protective factor, with a particular window of action around 4 weeks preconception and during the first trimester. These prenatal risks and protective mechanisms appear to involve G × E and potentially rGE. A variety of perinatal risks are related to offspring ASC risk, possibly reflecting rGE. Postnatal social factors (e.g. caregiver–infant interaction, severe early deprivation) during the first years of life may operate through rGE to influence the likelihood of manifesting a full ASC phenotype from a ‘prodromal’ phase (a proposal distinct to the discredited and harmful ‘refrigerator mother hypothesis’); and later postnatal risks, after the full manifestation of ASC, shape life span development through transactions mediated by rGE. There is no evidence that vaccination is a postnatal risk for ASC. Conclusions Future investigations should consider the specificity of risks for ASC versus other atypical neurodevelopmental trajectories, timing of risk and protective mechanisms, animal model systems to study mechanisms underlying gene–environment interplay, large-sample genome–envirome designs to address G × E and longitudinal studies to elucidate how rGE plays out over time. Clinical and public health implications are discussed. En ligne : http://dx.doi.org/10.1111/jcpp.12501 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=282 [article] Annual Research Review: The role of the environment in the developmental psychopathology of autism spectrum condition [texte imprimé] / William MANDY, Auteur ; Meng-Chuan LAI, Auteur . - p.271-292. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 57-3 (March 2016) . - p.271-292 Mots-clés : Autism spectrum condition  autism spectrum disorder  autism  Asperger's syndrome  genetics  environment  developmental psychopathology Index. décimale : PER Périodiques Résumé : Background Although autism spectrum condition (ASC) is strongly genetic in origin, accumulating evidence points to the critical roles of various environmental influences on its emergence and subsequent developmental course. Methods A developmental psychopathology framework was used to synthesise literature on environmental factors associated with the onset and course of ASC (based on a systematic search of the literature using PubMed, PsychInfo and Google Scholar databases). Particular emphasis was placed on gene–environment interplay, including gene–environment interaction (G × E) and gene–environment correlation (rGE). Results Before conception, advanced paternal and maternal ages may independently enhance offspring risk for ASC. Exogenous prenatal risks are evident (e.g. valproate and toxic chemicals) or possible (e.g. selective serotonin reuptake inhibitors), and processes endogenous to the materno-foeto-placental unit (e.g. maternal diabetes, enhanced steroidogenic activities and maternal immune activation) likely heighten offspring vulnerability to ASC. Folate intake is a prenatal protective factor, with a particular window of action around 4 weeks preconception and during the first trimester. These prenatal risks and protective mechanisms appear to involve G × E and potentially rGE. A variety of perinatal risks are related to offspring ASC risk, possibly reflecting rGE. Postnatal social factors (e.g. caregiver–infant interaction, severe early deprivation) during the first years of life may operate through rGE to influence the likelihood of manifesting a full ASC phenotype from a ‘prodromal’ phase (a proposal distinct to the discredited and harmful ‘refrigerator mother hypothesis’); and later postnatal risks, after the full manifestation of ASC, shape life span development through transactions mediated by rGE. There is no evidence that vaccination is a postnatal risk for ASC. Conclusions Future investigations should consider the specificity of risks for ASC versus other atypical neurodevelopmental trajectories, timing of risk and protective mechanisms, animal model systems to study mechanisms underlying gene–environment interplay, large-sample genome–envirome designs to address G × E and longitudinal studies to elucidate how rGE plays out over time. Clinical and public health implications are discussed. En ligne : http://dx.doi.org/10.1111/jcpp.12501 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=282

Are Prenatal Ultrasound Scans Associated with the Autism Phenotype? Follow-up of a Randomised Controlled Trial / Yonit K. STOCH in Journal of Autism and Developmental Disorders, 42-12 (December 2012)  

Public ISBD [article]  inJournal of Autism and Developmental Disorders > 42-12 (December 2012) . - p.2693-2701 Titre : Are Prenatal Ultrasound Scans Associated with the Autism Phenotype? Follow-up of a Randomised Controlled Trial Type de document : texte imprimé Auteurs : Yonit K. STOCH, Auteur ; Cori J. WILLIAMS, Auteur ; Joanna GRANICH, Auteur ; Anna HUNT, Auteur ; Lou I. LANDAU, Auteur ; John P. NEWNHAM, Auteur ; Andrew J.O. WHITEHOUSE, Auteur Article en page(s) : p.2693-2701 Langues : Anglais (eng) Mots-clés : Autism spectrum disorder  Autism  Prenatal  Ultrasonography  Obstetric  Environment Index. décimale : PER Périodiques Résumé : An existing randomised controlled trial was used to investigate whether multiple ultrasound scans may be associated with the autism phenotype. From 2,834 single pregnancies, 1,415 were selected at random to receive ultrasound imaging and continuous wave Doppler flow studies at five points throughout pregnancy (Intensive) and 1,419 to receive a single imaging scan at 18 weeks (Regular), with further scans only as indicated on clinical grounds. There was no significant difference in the rate of Autism Spectrum Disorder between the Regular (9/1,125, 0.8 %) and Intensive (7/1,167, 0.6 %) groups, nor a difference between groups in the level of autistic-like traits in early adulthood. There is no clear link between the frequency and timing of prenatal ultrasound scans and the autism phenotype. En ligne : http://dx.doi.org/10.1007/s10803-012-1526-8 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=184 [article] Are Prenatal Ultrasound Scans Associated with the Autism Phenotype? Follow-up of a Randomised Controlled Trial [texte imprimé] / Yonit K. STOCH, Auteur ; Cori J. WILLIAMS, Auteur ; Joanna GRANICH, Auteur ; Anna HUNT, Auteur ; Lou I. LANDAU, Auteur ; John P. NEWNHAM, Auteur ; Andrew J.O. WHITEHOUSE, Auteur . - p.2693-2701. Langues : Anglais (eng) in Journal of Autism and Developmental Disorders > 42-12 (December 2012) . - p.2693-2701 Mots-clés : Autism spectrum disorder  Autism  Prenatal  Ultrasonography  Obstetric  Environment Index. décimale : PER Périodiques Résumé : An existing randomised controlled trial was used to investigate whether multiple ultrasound scans may be associated with the autism phenotype. From 2,834 single pregnancies, 1,415 were selected at random to receive ultrasound imaging and continuous wave Doppler flow studies at five points throughout pregnancy (Intensive) and 1,419 to receive a single imaging scan at 18 weeks (Regular), with further scans only as indicated on clinical grounds. There was no significant difference in the rate of Autism Spectrum Disorder between the Regular (9/1,125, 0.8 %) and Intensive (7/1,167, 0.6 %) groups, nor a difference between groups in the level of autistic-like traits in early adulthood. There is no clear link between the frequency and timing of prenatal ultrasound scans and the autism phenotype. En ligne : http://dx.doi.org/10.1007/s10803-012-1526-8 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=184

Are thyroid hormone concentrations at birth associated with subsequent autism diagnosis? / Sumi HOSHIKO in Autism Research, 4-6 (December 2011)  

Public ISBD [article]  inAutism Research > 4-6 (December 2011) . - p.456-463 Titre : Are thyroid hormone concentrations at birth associated with subsequent autism diagnosis? Type de document : texte imprimé Auteurs : Sumi HOSHIKO, Auteur ; Judith K. GRETHER, Auteur ; Gayle C. WINDHAM, Auteur ; Daniel W. SMITH, Auteur ; Karen FESSEL, Auteur Année de publication : 2012 Article en page(s) : p.456-463 Langues : Anglais (eng) Mots-clés : epidemiology  autism  thyroid  environment  hormones Index. décimale : PER Périodiques Résumé : Thyroid hormones substantially influence central nervous system development during gestation. We hypothesized that perturbations of early thyroid profiles may contribute to the development of autism spectrum disorders (ASD). Thyroid pathways could provide a mechanism by which environmental factors that affect the thyroid system may impact autism occurrence or phenotypic expression. We investigated whether thyroxine (T4) levels at birth are associated with subsequent ASD, using two existing California study groups in multivariate analysis. One study group included children born in the San Francisco Bay Area in 1994, with cases identified through the California Department of Developmental Services (DDS) and/or the Kaiser Permanente Medical Care Program of Northern California (244 cases, 266 controls); the other included children born in California in 1995, with cases identified through DDS (310 cases, 518 controls). Matched controls were selected from birth certificate records. This exploratory analysis suggested that infants with very low T4 (<3rd percentile) may have higher ASD risk, although results reached statistical significance only for the 1995 study group (1995: OR = 2.74 (95% CI 1.30–5.75; 1994: OR = 1.71 (95% CI 0.57–5.19). A variety of alternate analyses were conducted with available data, without further resolution of the difference between the two study groups. The results of our study indicate that further studies are warranted to investigate whether thyroid hormone perturbations play a role in the development of ASD by evaluating additional potential confounders and genotype or phenotype in larger studies. En ligne : http://dx.doi.org/10.1002/aur.219 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=151 [article] Are thyroid hormone concentrations at birth associated with subsequent autism diagnosis? [texte imprimé] / Sumi HOSHIKO, Auteur ; Judith K. GRETHER, Auteur ; Gayle C. WINDHAM, Auteur ; Daniel W. SMITH, Auteur ; Karen FESSEL, Auteur . - 2012 . - p.456-463. Langues : Anglais (eng) in Autism Research > 4-6 (December 2011) . - p.456-463 Mots-clés : epidemiology  autism  thyroid  environment  hormones Index. décimale : PER Périodiques Résumé : Thyroid hormones substantially influence central nervous system development during gestation. We hypothesized that perturbations of early thyroid profiles may contribute to the development of autism spectrum disorders (ASD). Thyroid pathways could provide a mechanism by which environmental factors that affect the thyroid system may impact autism occurrence or phenotypic expression. We investigated whether thyroxine (T4) levels at birth are associated with subsequent ASD, using two existing California study groups in multivariate analysis. One study group included children born in the San Francisco Bay Area in 1994, with cases identified through the California Department of Developmental Services (DDS) and/or the Kaiser Permanente Medical Care Program of Northern California (244 cases, 266 controls); the other included children born in California in 1995, with cases identified through DDS (310 cases, 518 controls). Matched controls were selected from birth certificate records. This exploratory analysis suggested that infants with very low T4 (<3rd percentile) may have higher ASD risk, although results reached statistical significance only for the 1995 study group (1995: OR = 2.74 (95% CI 1.30–5.75; 1994: OR = 1.71 (95% CI 0.57–5.19). A variety of alternate analyses were conducted with available data, without further resolution of the difference between the two study groups. The results of our study indicate that further studies are warranted to investigate whether thyroid hormone perturbations play a role in the development of ASD by evaluating additional potential confounders and genotype or phenotype in larger studies. En ligne : http://dx.doi.org/10.1002/aur.219 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=151

Brief Report: Reliability of the Participation and Sensory Environment Questionnaire: Home Scales / Beth PFEIFFER in Journal of Autism and Developmental Disorders, 48-7 (July 2018)  

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Chaotic homes and school achievement: a twin study / Ken B. HANSCOMBE in Journal of Child Psychology and Psychiatry, 52-11 (November 2011)  

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Commentary: Not just genes – reclaiming a role for environmental influences on aetiology and outcome in autism. A commentary on Mandy and Lai (2016) / Tony CHARMAN in Journal of Child Psychology and Psychiatry, 57-3 (March 2016)  

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Dyslexia-A Learning Difference / I.C.J. ADUBASIM in Autism - Open Access, 7-1 ([01/01/2017])  

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Editorial: ADHD persistence – the interplay of genes, socioeconomic context, and symptom domains over development / Phoebe THOMSON in Journal of Child Psychology and Psychiatry, 67-5 (May 2026)  

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