Brain functional connectivity correlates of autism diagnosis and familial liability in 24-month-olds / John R. Jr PRUETT in Journal of Neurodevelopmental Disorders, 17 (2025)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 17 (2025) Titre : Brain functional connectivity correlates of autism diagnosis and familial liability in 24-month-olds Type de document : texte imprimé Auteurs : John R. Jr PRUETT, Auteur ; Alexandre A. TODOROV, Auteur ; Zoë W. HAWKS, Auteur ; Muhamed TALOVIĆ, Auteur ; Tomoyuki NISHINO, Auteur ; Steven E. PETERSEN, Auteur ; Savannah DAVIS, Auteur ; Lyn STAHL, Auteur ; Kelly N. BOTTERON, Auteur ; John N. CONSTANTINO, Auteur ; Stephen R. DAGER, Auteur ; Jed T. ELISON, Auteur ; Annette M. ESTES, Auteur ; Alan C. EVANS, Auteur ; Guido GERIG, Auteur ; Jessica B. GIRAULT, Auteur ; Heather HAZLETT, Auteur ; Leigh MACINTYRE, Auteur ; Natasha MARRUS, Auteur ; Robert C. MCKINSTRY, Auteur ; Juhi PANDEY, Auteur ; Robert T. SCHULTZ, Auteur ; William D. SHANNON, Auteur ; Mark D. SHEN, Auteur ; Abraham Z. SNYDER, Auteur ; Martin STYNER, Auteur ; Jason J. WOLFF, Auteur ; Lonnie ZWAIGENBAUM, Auteur ; Joseph PIVEN, Auteur ; THE IBIS NETWORK, Auteur Langues : Anglais (eng) Mots-clés : Humans  Male  Female  Magnetic Resonance Imaging  Autism Spectrum Disorder/physiopathology/diagnostic imaging  Child, Preschool  Brain/physiopathology/diagnostic imaging  Support Vector Machine  Connectome  Nerve Net/physiopathology/diagnostic imaging  Infant  Siblings  Default mode network  Familial  Functional connectivity  MRI  reviewed and approved by the internal review boards of Washington University  School of Medicine, IRB IDs 201103140 and 201301110, the University of  Washington, IRB IDs 12317 and STUDY00012991, The Children’s Hospital of  Philadelphia, IRB ID 07-005689, and the University of North Carolina at Chapel  Hill, IRB ID 05-2293. Informed consent was signed by all study participants.  Competing interests: Dr. Robert McKinstry serves on the advisory board of Nous  Imaging, Inc. and receives funding for meals and travel from Siemens Healthineers  and Philips Healthcare. Abraham Z. Snyder is a consultant for Sora Neuroscience,  LLC. All other authors report no financial relationships with commercial  interests. Index. décimale : PER Périodiques Résumé : BACKGROUND: fcMRI correlates of autism spectrum disorder (ASD) diagnosis and familial liability were studied in 24-month-olds at high (older affected sibling) and low familial likelihood for ASD. METHODS: fcMRI comparisons of high-familial-likelihood (HL) ASD-positive (HLP, N = 23) and ASD-negative (HLN, N = 91), and low-likelihood ASD-negative (LLN, N = 27) 24-month-olds from the Infant Brain Imaging Study (IBIS) Network were conducted, employing object oriented data analysis (OODA), support vector machine (SVM) classification, and network-level fcMRI enrichment analyses. RESULTS: OODA (alpha = 0.0167, 3 comparisons) revealed differences in HLP and LLN fcMRI matrices (p = 0.012), but none for HLP versus HLN (p = 0.047) nor HLN versus LLN (p = 0.225). SVM distinguished HLP from HLN (accuracy = 99%, PPV = 96%, NPV = 100%), based on connectivity involving many networks. SVM accurately classified (non-training) LLN subjects with 100% accuracy. Enrichment analyses identified a cross-group fcMRI difference in the posterior cingulate default mode network 1 (pcDMN1)- temporal default mode network (tDMN) pair (p = 0.0070). Functional connectivity for implicated connections in these networks was consistently lower in HLP and HLN than in LLN (p = 0.0461 and 0.0004). HLP did not differ from HLN (p = 0.2254). Secondary testing showed HL children with low ASD behaviors still differed from LLN (p = 0.0036). CONCLUSIONS: 24-month-old high-familial-likelihood infants show reduced intra-DMN connectivity, a potential neural finding related to familial liability, while widely distributed functional connections correlate with ASD diagnosis. En ligne : https://dx.doi.org/10.1186/s11689-025-09621-9 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=576 [article] Brain functional connectivity correlates of autism diagnosis and familial liability in 24-month-olds [texte imprimé] / John R. Jr PRUETT, Auteur ; Alexandre A. TODOROV, Auteur ; Zoë W. HAWKS, Auteur ; Muhamed TALOVIĆ, Auteur ; Tomoyuki NISHINO, Auteur ; Steven E. PETERSEN, Auteur ; Savannah DAVIS, Auteur ; Lyn STAHL, Auteur ; Kelly N. BOTTERON, Auteur ; John N. CONSTANTINO, Auteur ; Stephen R. DAGER, Auteur ; Jed T. ELISON, Auteur ; Annette M. ESTES, Auteur ; Alan C. EVANS, Auteur ; Guido GERIG, Auteur ; Jessica B. GIRAULT, Auteur ; Heather HAZLETT, Auteur ; Leigh MACINTYRE, Auteur ; Natasha MARRUS, Auteur ; Robert C. MCKINSTRY, Auteur ; Juhi PANDEY, Auteur ; Robert T. SCHULTZ, Auteur ; William D. SHANNON, Auteur ; Mark D. SHEN, Auteur ; Abraham Z. SNYDER, Auteur ; Martin STYNER, Auteur ; Jason J. WOLFF, Auteur ; Lonnie ZWAIGENBAUM, Auteur ; Joseph PIVEN, Auteur ; THE IBIS NETWORK, Auteur. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 17 (2025) Mots-clés : Humans  Male  Female  Magnetic Resonance Imaging  Autism Spectrum Disorder/physiopathology/diagnostic imaging  Child, Preschool  Brain/physiopathology/diagnostic imaging  Support Vector Machine  Connectome  Nerve Net/physiopathology/diagnostic imaging  Infant  Siblings  Default mode network  Familial  Functional connectivity  MRI  reviewed and approved by the internal review boards of Washington University  School of Medicine, IRB IDs 201103140 and 201301110, the University of  Washington, IRB IDs 12317 and STUDY00012991, The Children’s Hospital of  Philadelphia, IRB ID 07-005689, and the University of North Carolina at Chapel  Hill, IRB ID 05-2293. Informed consent was signed by all study participants.  Competing interests: Dr. Robert McKinstry serves on the advisory board of Nous  Imaging, Inc. and receives funding for meals and travel from Siemens Healthineers  and Philips Healthcare. Abraham Z. Snyder is a consultant for Sora Neuroscience,  LLC. All other authors report no financial relationships with commercial  interests. Index. décimale : PER Périodiques Résumé : BACKGROUND: fcMRI correlates of autism spectrum disorder (ASD) diagnosis and familial liability were studied in 24-month-olds at high (older affected sibling) and low familial likelihood for ASD. METHODS: fcMRI comparisons of high-familial-likelihood (HL) ASD-positive (HLP, N = 23) and ASD-negative (HLN, N = 91), and low-likelihood ASD-negative (LLN, N = 27) 24-month-olds from the Infant Brain Imaging Study (IBIS) Network were conducted, employing object oriented data analysis (OODA), support vector machine (SVM) classification, and network-level fcMRI enrichment analyses. RESULTS: OODA (alpha = 0.0167, 3 comparisons) revealed differences in HLP and LLN fcMRI matrices (p = 0.012), but none for HLP versus HLN (p = 0.047) nor HLN versus LLN (p = 0.225). SVM distinguished HLP from HLN (accuracy = 99%, PPV = 96%, NPV = 100%), based on connectivity involving many networks. SVM accurately classified (non-training) LLN subjects with 100% accuracy. Enrichment analyses identified a cross-group fcMRI difference in the posterior cingulate default mode network 1 (pcDMN1)- temporal default mode network (tDMN) pair (p = 0.0070). Functional connectivity for implicated connections in these networks was consistently lower in HLP and HLN than in LLN (p = 0.0461 and 0.0004). HLP did not differ from HLN (p = 0.2254). Secondary testing showed HL children with low ASD behaviors still differed from LLN (p = 0.0036). CONCLUSIONS: 24-month-old high-familial-likelihood infants show reduced intra-DMN connectivity, a potential neural finding related to familial liability, while widely distributed functional connections correlate with ASD diagnosis. En ligne : https://dx.doi.org/10.1186/s11689-025-09621-9 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=576

Brain volumes, cognitive, and adaptive skills in school-age children with Down syndrome / Rebecca GRZADZINSKI in Journal of Neurodevelopmental Disorders, 16 (2024)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 16 (2024) Titre : Brain volumes, cognitive, and adaptive skills in school-age children with Down syndrome Type de document : texte imprimé Auteurs : Rebecca GRZADZINSKI, Auteur ; Kattia MATA, Auteur ; Ambika S. BHATT, Auteur ; Alapika JATKAR, Auteur ; Dea GARIC, Auteur ; Mark D. SHEN, Auteur ; Jessica B. GIRAULT, Auteur ; Tanya ST JOHN, Auteur ; Juhi PANDEY, Auteur ; Lonnie ZWAIGENBAUM, Auteur ; Annette ESTES, Auteur ; Audrey M. SHEN, Auteur ; Stephen DAGER, Auteur ; Robert SCHULTZ, Auteur ; Kelly BOTTERON, Auteur ; Natasha MARRUS, Auteur ; Martin STYNER, Auteur ; Alan EVANS, Auteur ; Sun Hyung KIM, Auteur ; Robert MCKINSTRY, Auteur ; Guido GERIG, Auteur ; Joseph PIVEN, Auteur ; Heather HAZLETT, Auteur ; IBIS NETWORK, Auteur Langues : Anglais (eng) Mots-clés : Humans  Down Syndrome/diagnostic imaging/physiopathology/pathology  Male  Female  Child  Magnetic Resonance Imaging  Adaptation, Psychological/physiology  Cognition/physiology  Brain/diagnostic imaging/pathology/physiopathology  Autism Spectrum Disorder/diagnostic imaging/physiopathology/pathology  Organ Size  Cerebellum/diagnostic imaging/pathology/physiopathology  Adaptive  Autism spectrum disorder  Brain volumes  Cognitive  Cortical volumes  Down syndrome  Intellectual disability  Mri  Neurobehavioral/behavioral profiles  Neurodevelopmental disorder  Neuroimaging  School-age children  in this work was approved by the local Institutional Review Board. Consent for  publication: All authors have reviewed the manuscript and approved it for  publication. Competing interests: The authors declare no competing interests. Index. décimale : PER Périodiques Résumé : BACKGROUND: Down syndrome (DS) is the most common congenital neurodevelopmental disorder, present in about 1 in every 700 live births. Despite its prevalence, literature exploring the neurobiology underlying DS and how this neurobiology is related to behavior is limited. This study fills this gap by examining cortical volumes and behavioral correlates in school-age children with DS. METHODS: School-age children (mean = 9.7 years ± 1.1) underwent comprehensive assessments, including cognitive and adaptive assessments, as well as an MRI scan without the use of sedation. Children with DS (n = 35) were compared to available samples of typically developing (TD; n = 80) and ASD children (n = 29). ANOVAs were conducted to compare groups on cognitive and adaptive assessments. ANCOVAs (covarying for age, sex, and total cerebral volume; TCV) compared cortical brain volumes between groups. Correlations between behavioral metrics and cortical and cerebellar volumes (separately for gray (GM) and white matter (WM)) were conducted separately by group. RESULTS: As expected, children with DS had significantly lower cognitive skills compared to ASD and TD children. Daily Living adaptive skills were comparable between ASD children and children with DS, and both groups scored lower than TD children. Children with DS exhibited a smaller TCV compared to ASD and TD children. Additionally, when controlling for TCV, age, and sex, children with DS had significantly smaller total GM and tissue volumes. Cerebellum volumes were significantly correlated with Daily Living adaptive behaviors in the DS group only. CONCLUSIONS: Despite children with DS exhibiting lower cognitive skills and smaller brain volume overall than children with ASD, their deficits in Socialization and Daily Living adaptive skills are comparable. Differences in lobar volumes (e.g., Right Frontal GM/WM, Left Frontal WM, and Left and Right Temporal WM) were observed above and beyond overall differences in total volume. The correlation between cerebellum volumes and Daily Living adaptive behaviors in the DS group provides a novel area to explore in future research. En ligne : https://dx.doi.org/10.1186/s11689-024-09581-6 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=576 [article] Brain volumes, cognitive, and adaptive skills in school-age children with Down syndrome [texte imprimé] / Rebecca GRZADZINSKI, Auteur ; Kattia MATA, Auteur ; Ambika S. BHATT, Auteur ; Alapika JATKAR, Auteur ; Dea GARIC, Auteur ; Mark D. SHEN, Auteur ; Jessica B. GIRAULT, Auteur ; Tanya ST JOHN, Auteur ; Juhi PANDEY, Auteur ; Lonnie ZWAIGENBAUM, Auteur ; Annette ESTES, Auteur ; Audrey M. SHEN, Auteur ; Stephen DAGER, Auteur ; Robert SCHULTZ, Auteur ; Kelly BOTTERON, Auteur ; Natasha MARRUS, Auteur ; Martin STYNER, Auteur ; Alan EVANS, Auteur ; Sun Hyung KIM, Auteur ; Robert MCKINSTRY, Auteur ; Guido GERIG, Auteur ; Joseph PIVEN, Auteur ; Heather HAZLETT, Auteur ; IBIS NETWORK, Auteur. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 16 (2024) Mots-clés : Humans  Down Syndrome/diagnostic imaging/physiopathology/pathology  Male  Female  Child  Magnetic Resonance Imaging  Adaptation, Psychological/physiology  Cognition/physiology  Brain/diagnostic imaging/pathology/physiopathology  Autism Spectrum Disorder/diagnostic imaging/physiopathology/pathology  Organ Size  Cerebellum/diagnostic imaging/pathology/physiopathology  Adaptive  Autism spectrum disorder  Brain volumes  Cognitive  Cortical volumes  Down syndrome  Intellectual disability  Mri  Neurobehavioral/behavioral profiles  Neurodevelopmental disorder  Neuroimaging  School-age children  in this work was approved by the local Institutional Review Board. Consent for  publication: All authors have reviewed the manuscript and approved it for  publication. Competing interests: The authors declare no competing interests. Index. décimale : PER Périodiques Résumé : BACKGROUND: Down syndrome (DS) is the most common congenital neurodevelopmental disorder, present in about 1 in every 700 live births. Despite its prevalence, literature exploring the neurobiology underlying DS and how this neurobiology is related to behavior is limited. This study fills this gap by examining cortical volumes and behavioral correlates in school-age children with DS. METHODS: School-age children (mean = 9.7 years ± 1.1) underwent comprehensive assessments, including cognitive and adaptive assessments, as well as an MRI scan without the use of sedation. Children with DS (n = 35) were compared to available samples of typically developing (TD; n = 80) and ASD children (n = 29). ANOVAs were conducted to compare groups on cognitive and adaptive assessments. ANCOVAs (covarying for age, sex, and total cerebral volume; TCV) compared cortical brain volumes between groups. Correlations between behavioral metrics and cortical and cerebellar volumes (separately for gray (GM) and white matter (WM)) were conducted separately by group. RESULTS: As expected, children with DS had significantly lower cognitive skills compared to ASD and TD children. Daily Living adaptive skills were comparable between ASD children and children with DS, and both groups scored lower than TD children. Children with DS exhibited a smaller TCV compared to ASD and TD children. Additionally, when controlling for TCV, age, and sex, children with DS had significantly smaller total GM and tissue volumes. Cerebellum volumes were significantly correlated with Daily Living adaptive behaviors in the DS group only. CONCLUSIONS: Despite children with DS exhibiting lower cognitive skills and smaller brain volume overall than children with ASD, their deficits in Socialization and Daily Living adaptive skills are comparable. Differences in lobar volumes (e.g., Right Frontal GM/WM, Left Frontal WM, and Left and Right Temporal WM) were observed above and beyond overall differences in total volume. The correlation between cerebellum volumes and Daily Living adaptive behaviors in the DS group provides a novel area to explore in future research. En ligne : https://dx.doi.org/10.1186/s11689-024-09581-6 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=576

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

Developmental outcomes of early adverse care on amygdala functional connectivity in nonhuman primates / Elyse L. MORIN in Development and Psychopathology, 32-5 (December 2020)  

Public ISBD [article]  inDevelopment and Psychopathology > 32-5 (December 2020) . - p.1579-1596 Titre : Developmental outcomes of early adverse care on amygdala functional connectivity in nonhuman primates Type de document : texte imprimé Auteurs : Elyse L. MORIN, Auteur ; Brittany R. HOWELL, Auteur ; Eric FECZKO, Auteur ; Eric A. EARL, Auteur ; Melanie PINCUS, Auteur ; Katherine REDING, Auteur ; Zsofia A. KOVACS-BALINT, Auteur ; Jerrold S. MEYER, Auteur ; Martin STYNER, Auteur ; Damien A. FAIR, Auteur ; Mar M. SANCHEZ, Auteur Article en page(s) : p.1579-1596 Langues : Anglais (eng) Mots-clés : Adolescent  *Amygdala/diagnostic imaging  Animals  Brain  Child  Female  Humans  Magnetic Resonance Imaging  Neural Pathways/diagnostic imaging  *Prefrontal Cortex/diagnostic imaging  Pregnancy  Primates  *amygdala functional connectivity  *childhood maltreatment  *early life stress  *prefrontal cortex  *rhesus monkey Index. décimale : PER Périodiques Résumé : Despite the strong link between childhood maltreatment and psychopathology, the underlying neurodevelopmental mechanisms are poorly understood and difficult to disentangle from heritable and prenatal factors. This study used a translational macaque model of infant maltreatment in which the adverse experience occurs in the first months of life, during intense maturation of amygdala circuits important for stress and emotional regulation. Thus, we examined the developmental impact of maltreatment on amygdala functional connectivity (FC) longitudinally, from infancy through the juvenile period. Using resting state functional magnetic resonance imaging (MRI) we performed amygdala-prefrontal cortex (PFC) region-of-interest and exploratory whole-brain amygdala FC analyses. The latter showed (a) developmental increases in amygdala FC with many regions, likely supporting increased processing of socioemotional-relevant stimuli with age; and (b) maltreatment effects on amygdala coupling with arousal and stress brain regions (locus coeruleus, laterodorsal tegmental area) that emerged with age. Maltreated juveniles showed weaker FC than controls, which was negatively associated with infant hair cortisol concentrations. Findings from the region-of-interest analysis also showed weaker amygdala FC with PFC regions in maltreated animals than controls since infancy, whereas bilateral amygdala FC was stronger in maltreated animals. These effects on amygdala FC development may underlie the poor behavioral outcomes associated with this adverse experience. En ligne : http://dx.doi.org/10.1017/s0954579420001133 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=437 [article] Developmental outcomes of early adverse care on amygdala functional connectivity in nonhuman primates [texte imprimé] / Elyse L. MORIN, Auteur ; Brittany R. HOWELL, Auteur ; Eric FECZKO, Auteur ; Eric A. EARL, Auteur ; Melanie PINCUS, Auteur ; Katherine REDING, Auteur ; Zsofia A. KOVACS-BALINT, Auteur ; Jerrold S. MEYER, Auteur ; Martin STYNER, Auteur ; Damien A. FAIR, Auteur ; Mar M. SANCHEZ, Auteur . - p.1579-1596. Langues : Anglais (eng) in Development and Psychopathology > 32-5 (December 2020) . - p.1579-1596 Mots-clés : Adolescent  *Amygdala/diagnostic imaging  Animals  Brain  Child  Female  Humans  Magnetic Resonance Imaging  Neural Pathways/diagnostic imaging  *Prefrontal Cortex/diagnostic imaging  Pregnancy  Primates  *amygdala functional connectivity  *childhood maltreatment  *early life stress  *prefrontal cortex  *rhesus monkey Index. décimale : PER Périodiques Résumé : Despite the strong link between childhood maltreatment and psychopathology, the underlying neurodevelopmental mechanisms are poorly understood and difficult to disentangle from heritable and prenatal factors. This study used a translational macaque model of infant maltreatment in which the adverse experience occurs in the first months of life, during intense maturation of amygdala circuits important for stress and emotional regulation. Thus, we examined the developmental impact of maltreatment on amygdala functional connectivity (FC) longitudinally, from infancy through the juvenile period. Using resting state functional magnetic resonance imaging (MRI) we performed amygdala-prefrontal cortex (PFC) region-of-interest and exploratory whole-brain amygdala FC analyses. The latter showed (a) developmental increases in amygdala FC with many regions, likely supporting increased processing of socioemotional-relevant stimuli with age; and (b) maltreatment effects on amygdala coupling with arousal and stress brain regions (locus coeruleus, laterodorsal tegmental area) that emerged with age. Maltreated juveniles showed weaker FC than controls, which was negatively associated with infant hair cortisol concentrations. Findings from the region-of-interest analysis also showed weaker amygdala FC with PFC regions in maltreated animals than controls since infancy, whereas bilateral amygdala FC was stronger in maltreated animals. These effects on amygdala FC development may underlie the poor behavioral outcomes associated with this adverse experience. En ligne : http://dx.doi.org/10.1017/s0954579420001133 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=437

Exposure to prenatal maternal distress and infant white matter neurodevelopment / Catherine H. DEMERS in Development and Psychopathology, 33-5 (December 2021)  

Public ISBD [article]  inDevelopment and Psychopathology > 33-5 (December 2021) . - p.1526-1538 Titre : Exposure to prenatal maternal distress and infant white matter neurodevelopment Type de document : texte imprimé Auteurs : Catherine H. DEMERS, Auteur ; Maria M. BAGONIS, Auteur ; Khalid AL-ALI, Auteur ; Sarah E. GARCIA, Auteur ; Martin A. STYNER, Auteur ; John H. GILMORE, Auteur ; M. Camille HOFFMAN, Auteur ; Benjamin L. HANKIN, Auteur ; Elysia Poggi DAVIS, Auteur Article en page(s) : p.1526-1538 Langues : Anglais (eng) Mots-clés : pregnancy  white matter microstructure  magnetic resonance imaging (MRI)  diffusion tensor imaging (DTI)  anxiety Index. décimale : PER Périodiques Résumé : The prenatal period represents a critical time for brain growth and development. These rapid neurological advances render the fetus susceptible to various influences with life-long implications for mental health. Maternal distress signals are a dominant early life influence, contributing to birth outcomes and risk for offspring psychopathology. This prospective longitudinal study evaluated the association between prenatal maternal distress and infant white matter microstructure. Participants included a racially and socioeconomically diverse sample of 85 mother–infant dyads. Prenatal distress was assessed at 17 and 29 weeks’ gestational age (GA). Infant structural data were collected via diffusion tensor imaging (DTI) at 42–45 weeks’ postconceptional age. Findings demonstrated that higher prenatal maternal distress at 29 weeks’ GA was associated with increased fractional anisotropy, b = .283, t(64) = 2.319, p = .024, and with increased axial diffusivity, b = .254, t(64) = 2.067, p = .043, within the right anterior cingulate white matter tract. No other significant associations were found with prenatal distress exposure and tract fractional anisotropy or axial diffusivity at 29 weeks’ GA, or earlier in gestation. En ligne : http://dx.doi.org/10.1017/S0954579421000742 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=457 [article] Exposure to prenatal maternal distress and infant white matter neurodevelopment [texte imprimé] / Catherine H. DEMERS, Auteur ; Maria M. BAGONIS, Auteur ; Khalid AL-ALI, Auteur ; Sarah E. GARCIA, Auteur ; Martin A. STYNER, Auteur ; John H. GILMORE, Auteur ; M. Camille HOFFMAN, Auteur ; Benjamin L. HANKIN, Auteur ; Elysia Poggi DAVIS, Auteur . - p.1526-1538. Langues : Anglais (eng) in Development and Psychopathology > 33-5 (December 2021) . - p.1526-1538 Mots-clés : pregnancy  white matter microstructure  magnetic resonance imaging (MRI)  diffusion tensor imaging (DTI)  anxiety Index. décimale : PER Périodiques Résumé : The prenatal period represents a critical time for brain growth and development. These rapid neurological advances render the fetus susceptible to various influences with life-long implications for mental health. Maternal distress signals are a dominant early life influence, contributing to birth outcomes and risk for offspring psychopathology. This prospective longitudinal study evaluated the association between prenatal maternal distress and infant white matter microstructure. Participants included a racially and socioeconomically diverse sample of 85 mother–infant dyads. Prenatal distress was assessed at 17 and 29 weeks’ gestational age (GA). Infant structural data were collected via diffusion tensor imaging (DTI) at 42–45 weeks’ postconceptional age. Findings demonstrated that higher prenatal maternal distress at 29 weeks’ GA was associated with increased fractional anisotropy, b = .283, t(64) = 2.319, p = .024, and with increased axial diffusivity, b = .254, t(64) = 2.067, p = .043, within the right anterior cingulate white matter tract. No other significant associations were found with prenatal distress exposure and tract fractional anisotropy or axial diffusivity at 29 weeks’ GA, or earlier in gestation. En ligne : http://dx.doi.org/10.1017/S0954579421000742 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=457

Functional connectivity between the visual and salience networks and autistic social features at school-age / Jessica B. GIRAULT in Journal of Neurodevelopmental Disorders, 17 (2025)  

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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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