Cerebrospinal fluid and the early brain development of autism / Mark D. SHEN in Journal of Neurodevelopmental Disorders, 10-1 (December 2018)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 10-1 (December 2018) . - 39 p. Titre : Cerebrospinal fluid and the early brain development of autism Type de document : texte imprimé Auteurs : Mark D. SHEN, Auteur Année de publication : 2018 Article en page(s) : 39 p. Langues : Anglais (eng) Mots-clés : Autism spectrum disorder  Biomarkers  Brain development  Brain enlargement  Cerebrospinal fluid  Early risk signs  Extra-axial cerebrospinal fluid  Glymphatic system  Heterogeneity  Infancy  Lateral ventricles  Neural meningeal lymphatic system  Neuroinflammation  Stratification biomarker Index. décimale : PER Périodiques Résumé : BACKGROUND: There is currently a renaissance of interest in the many functions of cerebrospinal fluid (CSF). Altered flow of CSF, for example, has been shown to impair the clearance of pathogenic inflammatory proteins involved in neurodegenerative diseases, such as amyloid-beta. In addition, the role of CSF in the newly discovered lymphatic system of the brain has become a prominently researched area in clinical neuroscience, as CSF serves as a conduit between the central nervous system and immune system. MAIN BODY: This article will review the importance of CSF in regulating normal brain development and function, from the prenatal period throughout the lifespan, and highlight recent research that CSF abnormalities in autism spectrum disorder (ASD) are present in infancy, are detectable by conventional structural MRI, and could serve as an early indicator of altered neurodevelopment. CONCLUSION: The identification of early CSF abnormalities in children with ASD, along with emerging knowledge of the underlying pathogenic mechanisms, has the potential to serve as early stratification biomarkers that separate children with ASD into biological subtypes that share a common pathophysiology. Such subtypes could help parse the phenotypic heterogeneity of ASD and map on to targeted, biologically based treatments. En ligne : http://dx.doi.org/10.1186/s11689-018-9256-7 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=386 [article] Cerebrospinal fluid and the early brain development of autism [texte imprimé] / Mark D. SHEN, Auteur . - 2018 . - 39 p. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 10-1 (December 2018) . - 39 p. Mots-clés : Autism spectrum disorder  Biomarkers  Brain development  Brain enlargement  Cerebrospinal fluid  Early risk signs  Extra-axial cerebrospinal fluid  Glymphatic system  Heterogeneity  Infancy  Lateral ventricles  Neural meningeal lymphatic system  Neuroinflammation  Stratification biomarker Index. décimale : PER Périodiques Résumé : BACKGROUND: There is currently a renaissance of interest in the many functions of cerebrospinal fluid (CSF). Altered flow of CSF, for example, has been shown to impair the clearance of pathogenic inflammatory proteins involved in neurodegenerative diseases, such as amyloid-beta. In addition, the role of CSF in the newly discovered lymphatic system of the brain has become a prominently researched area in clinical neuroscience, as CSF serves as a conduit between the central nervous system and immune system. MAIN BODY: This article will review the importance of CSF in regulating normal brain development and function, from the prenatal period throughout the lifespan, and highlight recent research that CSF abnormalities in autism spectrum disorder (ASD) are present in infancy, are detectable by conventional structural MRI, and could serve as an early indicator of altered neurodevelopment. CONCLUSION: The identification of early CSF abnormalities in children with ASD, along with emerging knowledge of the underlying pathogenic mechanisms, has the potential to serve as early stratification biomarkers that separate children with ASD into biological subtypes that share a common pathophysiology. Such subtypes could help parse the phenotypic heterogeneity of ASD and map on to targeted, biologically based treatments. En ligne : http://dx.doi.org/10.1186/s11689-018-9256-7 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=386

Comparative profiling of white matter development in the human and mouse brain reveals volumetric deficits and delayed myelination in Angelman syndrome / Ridthi K-R PATEL ; Tasmai VULLI ; Audrey L SMITH ; Martin A. STYNER ; Li-Ming HSU ; Sung-Ho LEE ; Yen-Yu Ian SHIH ; Heather C. HAZLETT ; Mark D. SHEN ; Alain C BURETTE ; Benjamin D. PHILPOT in Molecular Autism, 15 (2024)  

Public ISBD [article]  inMolecular Autism > 15 (2024) . - 54 Titre : Comparative profiling of white matter development in the human and mouse brain reveals volumetric deficits and delayed myelination in Angelman syndrome Type de document : texte imprimé Auteurs : Ridthi K-R PATEL, Auteur ; Tasmai VULLI, Auteur ; Audrey L SMITH, Auteur ; Martin A. STYNER, Auteur ; Li-Ming HSU, Auteur ; Sung-Ho LEE, Auteur ; Yen-Yu Ian SHIH, Auteur ; Heather C. HAZLETT, Auteur ; Mark D. SHEN, Auteur ; Alain C BURETTE, Auteur ; Benjamin D. PHILPOT, Auteur Article en page(s) : 54 Langues : Anglais (eng) Mots-clés : Animals  *Angelman Syndrome/genetics/pathology/diagnostic imaging  *White Matter/diagnostic imaging/pathology  Humans  Female  Male  Child, Preschool  *Myelin Sheath/metabolism/pathology  Infant  Child  Mice  *Ubiquitin-Protein Ligases/genetics/metabolism  Magnetic Resonance Imaging  Brain/diagnostic imaging/pathology/metabolism  Disease Models, Animal  Organ Size  Mice, Knockout  Microcephaly  Myelin basic protein  Myelination  Ube3a  White matter  and treatment of animals followed institutional and NIH guidelines, and all  animal use protocols were reviewed and approved by the UNC Institutional Animal  Care and Use Committee. Parents of AS and NT individuals provided informed  consent, and the institutional review board approved the research protocol.  Competing interests: The authors declare no competing interests. Index. décimale : PER Périodiques Résumé : BACKGROUND: Angelman syndrome (AS), a severe neurodevelopmental disorder resulting from the loss of the maternal UBE3A gene, is marked by changes in the brain's white matter (WM). The extent of WM abnormalities seems to correlate with the severity of clinical symptoms, but these deficits are still poorly characterized or understood. This study provides the first large-scale measurement of WM volume reduction in children with AS. Furthermore, we probed the possibility of underlying WM neuropathology by examining the progression of myelination in an AS mouse model. METHODS: We conducted magnetic resonance imaging (MRI) on children with AS (n = 32) and neurotypical controls (n = 99) aged 0.5-12 years. In parallel, we examined myelination in postnatal Ube3a maternal-null mice (Ube3a(m-/p+); AS model), Ube3a paternal-null mice (Ube3a(m+/p-)), and wildtype controls (Ube3a(m+/p+)) using MRI, immunohistochemistry, western blotting, and electron microscopy. RESULTS: Our data revealed that AS individuals exhibit significant reductions in brain volume by ~ 1 year of age, and by 6-12 years of age WM is reduced by 26% and gray matter by 21%-approximately twice the reductions observed in the adult AS mouse model. Our AS mouse model saw a global delay in the onset of myelination, which normalized within days (likely corresponding to months or years in human development). This myelination delay is caused by the loss of UBE3A in neurons rather than UBE3A haploinsufficiency in oligodendrocytes. Interestingly, ultrastructural analyses did not reveal abnormalities in myelinated or unmyelinated axons. LIMITATIONS: It is difficult to extrapolate the timing and duration of the myelination delay observed in AS model mice to individuals with AS. CONCLUSIONS: This study reveals WM deficits as a hallmark in children with AS, demonstrating for the first time that these deficits are already apparent at 1 year of age. Parallel studies in a mouse model of AS show these deficits occur alongside the delayed onset of myelination, which results from the loss of neuronal (but not glial) UBE3A, though the causal relationship between these phenotypes remains to be determined. These findings emphasize the potential of WM as both a therapeutic target for interventions and a valuable biomarker for tracking the progression of AS and the effectiveness of potential treatments. En ligne : https://dx.doi.org/10.1186/s13229-024-00636-y Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=555 [article] Comparative profiling of white matter development in the human and mouse brain reveals volumetric deficits and delayed myelination in Angelman syndrome [texte imprimé] / Ridthi K-R PATEL, Auteur ; Tasmai VULLI, Auteur ; Audrey L SMITH, Auteur ; Martin A. STYNER, Auteur ; Li-Ming HSU, Auteur ; Sung-Ho LEE, Auteur ; Yen-Yu Ian SHIH, Auteur ; Heather C. HAZLETT, Auteur ; Mark D. SHEN, Auteur ; Alain C BURETTE, Auteur ; Benjamin D. PHILPOT, Auteur . - 54. Langues : Anglais (eng) in Molecular Autism > 15 (2024) . - 54 Mots-clés : Animals  *Angelman Syndrome/genetics/pathology/diagnostic imaging  *White Matter/diagnostic imaging/pathology  Humans  Female  Male  Child, Preschool  *Myelin Sheath/metabolism/pathology  Infant  Child  Mice  *Ubiquitin-Protein Ligases/genetics/metabolism  Magnetic Resonance Imaging  Brain/diagnostic imaging/pathology/metabolism  Disease Models, Animal  Organ Size  Mice, Knockout  Microcephaly  Myelin basic protein  Myelination  Ube3a  White matter  and treatment of animals followed institutional and NIH guidelines, and all  animal use protocols were reviewed and approved by the UNC Institutional Animal  Care and Use Committee. Parents of AS and NT individuals provided informed  consent, and the institutional review board approved the research protocol.  Competing interests: The authors declare no competing interests. Index. décimale : PER Périodiques Résumé : BACKGROUND: Angelman syndrome (AS), a severe neurodevelopmental disorder resulting from the loss of the maternal UBE3A gene, is marked by changes in the brain's white matter (WM). The extent of WM abnormalities seems to correlate with the severity of clinical symptoms, but these deficits are still poorly characterized or understood. This study provides the first large-scale measurement of WM volume reduction in children with AS. Furthermore, we probed the possibility of underlying WM neuropathology by examining the progression of myelination in an AS mouse model. METHODS: We conducted magnetic resonance imaging (MRI) on children with AS (n = 32) and neurotypical controls (n = 99) aged 0.5-12 years. In parallel, we examined myelination in postnatal Ube3a maternal-null mice (Ube3a(m-/p+); AS model), Ube3a paternal-null mice (Ube3a(m+/p-)), and wildtype controls (Ube3a(m+/p+)) using MRI, immunohistochemistry, western blotting, and electron microscopy. RESULTS: Our data revealed that AS individuals exhibit significant reductions in brain volume by ~ 1 year of age, and by 6-12 years of age WM is reduced by 26% and gray matter by 21%-approximately twice the reductions observed in the adult AS mouse model. Our AS mouse model saw a global delay in the onset of myelination, which normalized within days (likely corresponding to months or years in human development). This myelination delay is caused by the loss of UBE3A in neurons rather than UBE3A haploinsufficiency in oligodendrocytes. Interestingly, ultrastructural analyses did not reveal abnormalities in myelinated or unmyelinated axons. LIMITATIONS: It is difficult to extrapolate the timing and duration of the myelination delay observed in AS model mice to individuals with AS. CONCLUSIONS: This study reveals WM deficits as a hallmark in children with AS, demonstrating for the first time that these deficits are already apparent at 1 year of age. Parallel studies in a mouse model of AS show these deficits occur alongside the delayed onset of myelination, which results from the loss of neuronal (but not glial) UBE3A, though the causal relationship between these phenotypes remains to be determined. These findings emphasize the potential of WM as both a therapeutic target for interventions and a valuable biomarker for tracking the progression of AS and the effectiveness of potential treatments. En ligne : https://dx.doi.org/10.1186/s13229-024-00636-y Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=555

Early language exposure supports later language skills in infants with and without autism / Meghan R. SWANSON in Autism Research, 12-12 (December)  

Public ISBD [article]  inAutism Research > 12-12 (December) . - p.1784-1795 Titre : Early language exposure supports later language skills in infants with and without autism Type de document : texte imprimé Auteurs : Meghan R. SWANSON, Auteur ; Kevin DONOVAN, Auteur ; Sarah J. PATERSON, Auteur ; Jason J. WOLFF, Auteur ; Julia PARISH-MORRIS, Auteur ; Shoba S. MEERA, Auteur ; Linda R. WATSON, Auteur ; Annette M. ESTES, Auteur ; Natasha M. MARRUS, Auteur ; Jed T. ELISON, Auteur ; Mark D. SHEN, Auteur ; Heidi B. MCNEILLY, Auteur ; Leigh MACINTYRE, Auteur ; Lonnie ZWAIGENBAUM, Auteur ; Tanya ST JOHN, Auteur ; Kelly N. BOTTERON, Auteur ; Stephen R. DAGER, Auteur ; Joseph PIVEN, Auteur Année de publication : 2019 Article en page(s) : p.1784-1795 Langues : Anglais (eng) Mots-clés : Asd  caregiver speech  high familial risk  home language environment  infancy  language  socioeconomic status Index. décimale : PER Périodiques Résumé : The way that parents communicate with their typically developing infants is associated with later infant language development. Here we aim to show that these associations are observed in infants subsequently diagnosed with autism spectrum disorder (ASD). This study had three groups: high-familial-risk infants who did not have ASD (n = 46); high-familial-risk infants who had ASD (n = 14); and low-familial-risk infants who exhibited typical development (n = 36). All-day home language recordings were collected at 9 and 15 months, and language skills were assessed at 24 months. Across all infants in the study, including those with ASD, a richer home language environment (e.g., hearing more adult words and experiencing more conversational turns) at 9 and 15 months was associated with better language skills. Higher parental educational attainment was associated with a richer home language environment. Mediation analyses showed that the effect of education on child language skills was explained by the richness of the home language environment. Exploratory analyses revealed that typically developing infants experience an increase in caregiver-child conversational turns across 9-15 months, a pattern not seen in children with ASD. The current study shows that parent behavior during the earliest stages of life can have a significant impact on later development, highlighting the home language environment as means to support development in infants with ASD. Autism Res 2019, 12: 1784-1795. (c) 2019 International Society for Autism Research, Wiley Periodicals, Inc. LAY SUMMARY: It has long been understood that caregiver speech supports language skills in typically developing infants. In this study, parents of infants who were later diagnosed with ASD and parents of infants in the control groups completed all-day home language recordings. We found that for all infants in our study, those who heard more caregiver speech had better language skills later in life. Parental education level was also related to how much caregiver speech an infant experienced. En ligne : http://dx.doi.org/10.1002/aur.2163 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=413 [article] Early language exposure supports later language skills in infants with and without autism [texte imprimé] / Meghan R. SWANSON, Auteur ; Kevin DONOVAN, Auteur ; Sarah J. PATERSON, Auteur ; Jason J. WOLFF, Auteur ; Julia PARISH-MORRIS, Auteur ; Shoba S. MEERA, Auteur ; Linda R. WATSON, Auteur ; Annette M. ESTES, Auteur ; Natasha M. MARRUS, Auteur ; Jed T. ELISON, Auteur ; Mark D. SHEN, Auteur ; Heidi B. MCNEILLY, Auteur ; Leigh MACINTYRE, Auteur ; Lonnie ZWAIGENBAUM, Auteur ; Tanya ST JOHN, Auteur ; Kelly N. BOTTERON, Auteur ; Stephen R. DAGER, Auteur ; Joseph PIVEN, Auteur . - 2019 . - p.1784-1795. Langues : Anglais (eng) in Autism Research > 12-12 (December) . - p.1784-1795 Mots-clés : Asd  caregiver speech  high familial risk  home language environment  infancy  language  socioeconomic status Index. décimale : PER Périodiques Résumé : The way that parents communicate with their typically developing infants is associated with later infant language development. Here we aim to show that these associations are observed in infants subsequently diagnosed with autism spectrum disorder (ASD). This study had three groups: high-familial-risk infants who did not have ASD (n = 46); high-familial-risk infants who had ASD (n = 14); and low-familial-risk infants who exhibited typical development (n = 36). All-day home language recordings were collected at 9 and 15 months, and language skills were assessed at 24 months. Across all infants in the study, including those with ASD, a richer home language environment (e.g., hearing more adult words and experiencing more conversational turns) at 9 and 15 months was associated with better language skills. Higher parental educational attainment was associated with a richer home language environment. Mediation analyses showed that the effect of education on child language skills was explained by the richness of the home language environment. Exploratory analyses revealed that typically developing infants experience an increase in caregiver-child conversational turns across 9-15 months, a pattern not seen in children with ASD. The current study shows that parent behavior during the earliest stages of life can have a significant impact on later development, highlighting the home language environment as means to support development in infants with ASD. Autism Res 2019, 12: 1784-1795. (c) 2019 International Society for Autism Research, Wiley Periodicals, Inc. LAY SUMMARY: It has long been understood that caregiver speech supports language skills in typically developing infants. In this study, parents of infants who were later diagnosed with ASD and parents of infants in the control groups completed all-day home language recordings. We found that for all infants in our study, those who heard more caregiver speech had better language skills later in life. Parental education level was also related to how much caregiver speech an infant experienced. En ligne : http://dx.doi.org/10.1002/aur.2163 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=413

Evidence for differential alternative splicing in blood of young boys with autism spectrum disorders / Boryana STAMOVA in Molecular Autism, (September 2013)  

Public ISBD [article]  inMolecular Autism > (September 2013) Titre : Evidence for differential alternative splicing in blood of young boys with autism spectrum disorders Type de document : texte imprimé Auteurs : Boryana STAMOVA, Auteur ; Yingfang TIAN, Auteur ; Christine W. NORDAHL, Auteur ; Mark SHEN, Auteur ; Sally J. ROGERS, Auteur ; David G. AMARAL, Auteur ; Frank SHARP, Auteur Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Since RNA expression differences have been reported in autism spectrum disorder (ASD) for blood and brain, and differential alternative splicing (DAS) has been reported in ASD brains, we determined if there was DAS in blood mRNA of ASD subjects compared to typically developing (TD) controls, as well as in ASD subgroups related to cerebral volume. RNA from blood was processed on whole genome exon arrays for 2-4-year-old ASD and TD boys. An ANCOVA with age and batch as covariates was used to predict DAS for ALL ASD (n=30), ASD with normal total cerebral volumes (NTCV), and ASD with large total cerebral volumes (LTCV) compared to TD controls (n=20). A total of 53 genes were predicted to have DAS for ALL ASD versus TD, 169 genes for ASD_NTCV versus TD, 1 gene for ASD_LTCV versus TD, and 27 genes for ASD_LTCV versus ASD_NTCV. These differences were significant at P 0.05 after false discovery rate corrections for multiple comparisons (FDR 5% false positives). A number of the genes predicted to have DAS in ASD are known to regulate DAS (SFPQ, SRPK1, SRSF11, SRSF2IP, FUS, LSM14A). In addition, a number of genes with predicted DAS are involved in pathways implicated in previous ASD studies, such as ROS monocyte/macrophage, Natural Killer Cell, mTOR, and NGF signaling. The only pathways significant after multiple comparison corrections (FDR 0.05) were the Nrf2-mediated reactive oxygen species (ROS) oxidative response (superoxide dismutase 2, catalase, peroxiredoxin 1, PIK3C3, DNAJC17, microsomal glutathione S-transferase 3) and superoxide radical degradation (SOD2, CAT). These data support differences in alternative splicing of mRNA in blood of ASD subjects compared to TD controls that differ related to head size. The findings are preliminary, need to be replicated in independent cohorts, and predicted alternative splicing differences need to be confirmed using direct analytical methods. En ligne : http://dx.doi.org/10.1186/2040-2392-4-30 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=227 [article] Evidence for differential alternative splicing in blood of young boys with autism spectrum disorders [texte imprimé] / Boryana STAMOVA, Auteur ; Yingfang TIAN, Auteur ; Christine W. NORDAHL, Auteur ; Mark SHEN, Auteur ; Sally J. ROGERS, Auteur ; David G. AMARAL, Auteur ; Frank SHARP, Auteur. Langues : Anglais (eng) in Molecular Autism > (September 2013) Index. décimale : PER Périodiques Résumé : Since RNA expression differences have been reported in autism spectrum disorder (ASD) for blood and brain, and differential alternative splicing (DAS) has been reported in ASD brains, we determined if there was DAS in blood mRNA of ASD subjects compared to typically developing (TD) controls, as well as in ASD subgroups related to cerebral volume. RNA from blood was processed on whole genome exon arrays for 2-4-year-old ASD and TD boys. An ANCOVA with age and batch as covariates was used to predict DAS for ALL ASD (n=30), ASD with normal total cerebral volumes (NTCV), and ASD with large total cerebral volumes (LTCV) compared to TD controls (n=20). A total of 53 genes were predicted to have DAS for ALL ASD versus TD, 169 genes for ASD_NTCV versus TD, 1 gene for ASD_LTCV versus TD, and 27 genes for ASD_LTCV versus ASD_NTCV. These differences were significant at P 0.05 after false discovery rate corrections for multiple comparisons (FDR 5% false positives). A number of the genes predicted to have DAS in ASD are known to regulate DAS (SFPQ, SRPK1, SRSF11, SRSF2IP, FUS, LSM14A). In addition, a number of genes with predicted DAS are involved in pathways implicated in previous ASD studies, such as ROS monocyte/macrophage, Natural Killer Cell, mTOR, and NGF signaling. The only pathways significant after multiple comparison corrections (FDR 0.05) were the Nrf2-mediated reactive oxygen species (ROS) oxidative response (superoxide dismutase 2, catalase, peroxiredoxin 1, PIK3C3, DNAJC17, microsomal glutathione S-transferase 3) and superoxide radical degradation (SOD2, CAT). These data support differences in alternative splicing of mRNA in blood of ASD subjects compared to TD controls that differ related to head size. The findings are preliminary, need to be replicated in independent cohorts, and predicted alternative splicing differences need to be confirmed using direct analytical methods. En ligne : http://dx.doi.org/10.1186/2040-2392-4-30 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=227

Identifying and Responding to Gaps in the Academic Research Pipeline: Findings From the International Society for Autism Research (INSAR) Early Career Committee / Giacomo VIVANTI ; Subhashini JAYANATH ; Kimberly L.H. CARPENTER ; Mark D. SHEN ; Frederick SHIC ; Jill LOCKE in Autism Research, 18-4 (April 2025)  

Public ISBD [article]  inAutism Research > 18-4 (April 2025) . - p.717-724 Titre : Identifying and Responding to Gaps in the Academic Research Pipeline: Findings From the International Society for Autism Research (INSAR) Early Career Committee Type de document : texte imprimé Auteurs : Giacomo VIVANTI, Auteur ; Subhashini JAYANATH, Auteur ; Kimberly L.H. CARPENTER, Auteur ; Mark D. SHEN, Auteur ; Frederick SHIC, Auteur ; Jill LOCKE, Auteur Article en page(s) : p.717-724 Langues : Anglais (eng) Mots-clés : autism  career development  early career researcher  global training resources Index. décimale : PER Périodiques Résumé : ABSTRACT The International Society for Autism Research (INSAR) was established in 2001 with the purpose of providing researchers in the field of autism a specific venue to enhance the quality of multidisciplinary research and elevate the field among the sciences. The autism field and size of the society has now expanded greatly to include over 5000 members, 29% of whom identify as early career researchers. In 2016, a survey was conducted with these early career researchers to identify existing supports and areas of need necessary for a successful and sustained autism research career. Results clearly identified three areas of need: (1) networking opportunities with ?change makers,? including funding agencies, journal editors, and senior autism researchers; (2) ensuring early career researchers in the autism research field were diverse and representative of the world; and (3) support from senior researchers to help early career researchers secure their first independent grant and move through promotion. The INSAR Early Career Committee (ECC) was established and developed three initiatives to address the aforementioned gaps: Research Rapid Rounds, the Global Representatives Initiative Pilot (GRIP), and the Mentoring Initiative. The ECC has successfully connected over 34 early career researchers and 40 students/trainees to mentors in 19 unique countries through networking programs and events and has established representatives in seven different countries outside the US and UK. These initiatives are a step towards supporting early career academics in the autism field and bring together autism researchers from around the world to share their work and create professional collaborations to forge our field forward. En ligne : https://doi.org/10.1002/aur.70028 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=554 [article] Identifying and Responding to Gaps in the Academic Research Pipeline: Findings From the International Society for Autism Research (INSAR) Early Career Committee [texte imprimé] / Giacomo VIVANTI, Auteur ; Subhashini JAYANATH, Auteur ; Kimberly L.H. CARPENTER, Auteur ; Mark D. SHEN, Auteur ; Frederick SHIC, Auteur ; Jill LOCKE, Auteur . - p.717-724. Langues : Anglais (eng) in Autism Research > 18-4 (April 2025) . - p.717-724 Mots-clés : autism  career development  early career researcher  global training resources Index. décimale : PER Périodiques Résumé : ABSTRACT The International Society for Autism Research (INSAR) was established in 2001 with the purpose of providing researchers in the field of autism a specific venue to enhance the quality of multidisciplinary research and elevate the field among the sciences. The autism field and size of the society has now expanded greatly to include over 5000 members, 29% of whom identify as early career researchers. In 2016, a survey was conducted with these early career researchers to identify existing supports and areas of need necessary for a successful and sustained autism research career. Results clearly identified three areas of need: (1) networking opportunities with ?change makers,? including funding agencies, journal editors, and senior autism researchers; (2) ensuring early career researchers in the autism research field were diverse and representative of the world; and (3) support from senior researchers to help early career researchers secure their first independent grant and move through promotion. The INSAR Early Career Committee (ECC) was established and developed three initiatives to address the aforementioned gaps: Research Rapid Rounds, the Global Representatives Initiative Pilot (GRIP), and the Mentoring Initiative. The ECC has successfully connected over 34 early career researchers and 40 students/trainees to mentors in 19 unique countries through networking programs and events and has established representatives in seven different countries outside the US and UK. These initiatives are a step towards supporting early career academics in the autism field and bring together autism researchers from around the world to share their work and create professional collaborations to forge our field forward. En ligne : https://doi.org/10.1002/aur.70028 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=554

Methods for acquiring MRI data in children with autism spectrum disorder and intellectual impairment without the use of sedation / Christine W. NORDAHL in Journal of Neurodevelopmental Disorders, 8-1 (December 2016)  

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Neural circuitry at age 6 months associated with later repetitive behavior and sensory responsiveness in autism / Jason J. WOLFF in Molecular Autism, 8 (2017)  

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