Dépouillements

Neural Mechanisms of Reward Prediction Error in Autism Spectrum Disorder / Maya G. MOSNER in Autism Research and Treatment, 2019 (2019)  

Public ISBD [article]  inAutism Research and Treatment > 2019 (2019) . - 10 p. Titre : Neural Mechanisms of Reward Prediction Error in Autism Spectrum Disorder Type de document : Texte imprimé et/ou numérique Auteurs : Maya G. MOSNER, Auteur ; R. Edward MCLAURIN, Auteur ; Jessica L. KINARD, Auteur ; Shabnam HAKIMI, Auteur ; Jacob PARELMAN, Auteur ; Jasmine S. SHAH, Auteur ; Joshua BIZZELL, Auteur ; Rachel K. GREENE, Auteur ; Paul M. CERNASOV, Auteur ; Erin WALSH, Auteur ; Merideth A. ADDICOTT, Auteur ; Tory EISENLOHR-MOUL, Auteur ; R. McKell CARTER, Auteur ; Gabriel S. DICHTER, Auteur Article en page(s) : 10 p. Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Few studies have explored neural mechanisms of reward learning in ASD despite evidence of behavioral impairments of predictive abilities in ASD. To investigate the neural correlates of reward prediction errors in ASD, 16 adults with ASD and 14 typically developing controls performed a prediction error task during fMRI scanning. Results revealed greater activation in the ASD group in the left paracingulate gyrus during signed prediction errors and the left insula and right frontal pole during thresholded unsigned prediction errors. Findings support atypical neural processing of reward prediction errors in ASD in frontostriatal regions critical for prediction coding and reward learning. Results provide a neural basis for impairments in reward learning that may contribute to traits common in ASD (e.g., intolerance of unpredictability). En ligne : https://doi.org/10.1155/2019/5469191 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=402 [article] Neural Mechanisms of Reward Prediction Error in Autism Spectrum Disorder [Texte imprimé et/ou numérique] / Maya G. MOSNER, Auteur ; R. Edward MCLAURIN, Auteur ; Jessica L. KINARD, Auteur ; Shabnam HAKIMI, Auteur ; Jacob PARELMAN, Auteur ; Jasmine S. SHAH, Auteur ; Joshua BIZZELL, Auteur ; Rachel K. GREENE, Auteur ; Paul M. CERNASOV, Auteur ; Erin WALSH, Auteur ; Merideth A. ADDICOTT, Auteur ; Tory EISENLOHR-MOUL, Auteur ; R. McKell CARTER, Auteur ; Gabriel S. DICHTER, Auteur . - 10 p. Langues : Anglais (eng) in Autism Research and Treatment > 2019 (2019) . - 10 p. Index. décimale : PER Périodiques Résumé : Few studies have explored neural mechanisms of reward learning in ASD despite evidence of behavioral impairments of predictive abilities in ASD. To investigate the neural correlates of reward prediction errors in ASD, 16 adults with ASD and 14 typically developing controls performed a prediction error task during fMRI scanning. Results revealed greater activation in the ASD group in the left paracingulate gyrus during signed prediction errors and the left insula and right frontal pole during thresholded unsigned prediction errors. Findings support atypical neural processing of reward prediction errors in ASD in frontostriatal regions critical for prediction coding and reward learning. Results provide a neural basis for impairments in reward learning that may contribute to traits common in ASD (e.g., intolerance of unpredictability). En ligne : https://doi.org/10.1155/2019/5469191 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=402

Improving Outcome in Infantile Autism with Folate Receptor Autoimmunity and Nutritional Derangements: A Self-Controlled Trial / Vincent Th. RAMAEKERS in Autism Research and Treatment, 2019 (2019)  

Public ISBD [article]  inAutism Research and Treatment > 2019 (2019) . - 12p. Titre : Improving Outcome in Infantile Autism with Folate Receptor Autoimmunity and Nutritional Derangements: A Self-Controlled Trial Type de document : Texte imprimé et/ou numérique Auteurs : Vincent Th. RAMAEKERS, Auteur ; Jeffrey M. SEQUEIRA, Auteur ; Marco DIDUCA, Auteur ; Géraldine VRANCKEN, Auteur ; Aurore THOMAS, Auteur ; Céline PHILIPPE, Auteur ; Marie PETERS, Auteur ; Annick JADOT, Auteur ; Edward V. QUADROS, Auteur Article en page(s) : 12p. Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Background. In contrast to multiple rare monogenetic abnormalities, a common biomarker among children with infantile autism and their parents is the discovery of serum autoantibodies directed to the folate receptor alpha (FR?) localized at blood-brain and placental barriers, impairing physiologic folate transfer to the brain and fetus. Since outcome after behavioral intervention remains poor, a trial was designed to treat folate receptor alpha (FR?) autoimmunity combined with correction of deficient nutrients due to abnormal feeding habits. Methods. All participants with nonsyndromic infantile autism underwent a routine protocol measuring CBC, iron, vitamins, coenzyme Q10, metals, and trace elements. Serum FR? autoantibodies were assessed in patients, their parents, and healthy controls. A self-controlled therapeutic trial treated nutritional derangements with addition of high-dose folinic acid if FR? autoantibodies tested positive. The Childhood Autism Rating Scale (CARS) monitored at baseline and following 2 years of treatment was compared to the CARS of untreated autistic children serving as a reference. Results. In this self-controlled trial (82 children; mean age ± SD: 4.4 ± 2.3 years; male:female ratio: 4.8:1), FR? autoantibodies were found in 75.6 % of the children, 34.1 % of mothers, and 29.4 % of fathers versus 3.3 % in healthy controls. Compared to untreated patients with autism (n=84) whose CARS score remained unchanged, a 2-year treatment decreased the initial CARS score from severe (mean ± SD: 41.34 ± 6.47) to moderate or mild autism (mean ± SD: 34.35 ± 6.25; paired t-test p<0.0001), achieving complete recovery in 17/82 children (20.7 %). Prognosis became less favorable with the finding of higher FR? autoantibody titers, positive maternal FR? autoantibodies, or FR? antibodies in both parents. Conclusions. Correction of nutritional deficiencies combined with high-dose folinic acid improved outcome for autism, although the trend of a poor prognosis due to maternal FR? antibodies or FR? antibodies in both parents may warrant folinic acid intervention before conception and during pregnancy. En ligne : https://doi.org/10.1155/2019/7486431 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=402 [article] Improving Outcome in Infantile Autism with Folate Receptor Autoimmunity and Nutritional Derangements: A Self-Controlled Trial [Texte imprimé et/ou numérique] / Vincent Th. RAMAEKERS, Auteur ; Jeffrey M. SEQUEIRA, Auteur ; Marco DIDUCA, Auteur ; Géraldine VRANCKEN, Auteur ; Aurore THOMAS, Auteur ; Céline PHILIPPE, Auteur ; Marie PETERS, Auteur ; Annick JADOT, Auteur ; Edward V. QUADROS, Auteur . - 12p. Langues : Anglais (eng) in Autism Research and Treatment > 2019 (2019) . - 12p. Index. décimale : PER Périodiques Résumé : Background. In contrast to multiple rare monogenetic abnormalities, a common biomarker among children with infantile autism and their parents is the discovery of serum autoantibodies directed to the folate receptor alpha (FR?) localized at blood-brain and placental barriers, impairing physiologic folate transfer to the brain and fetus. Since outcome after behavioral intervention remains poor, a trial was designed to treat folate receptor alpha (FR?) autoimmunity combined with correction of deficient nutrients due to abnormal feeding habits. Methods. All participants with nonsyndromic infantile autism underwent a routine protocol measuring CBC, iron, vitamins, coenzyme Q10, metals, and trace elements. Serum FR? autoantibodies were assessed in patients, their parents, and healthy controls. A self-controlled therapeutic trial treated nutritional derangements with addition of high-dose folinic acid if FR? autoantibodies tested positive. The Childhood Autism Rating Scale (CARS) monitored at baseline and following 2 years of treatment was compared to the CARS of untreated autistic children serving as a reference. Results. In this self-controlled trial (82 children; mean age ± SD: 4.4 ± 2.3 years; male:female ratio: 4.8:1), FR? autoantibodies were found in 75.6 % of the children, 34.1 % of mothers, and 29.4 % of fathers versus 3.3 % in healthy controls. Compared to untreated patients with autism (n=84) whose CARS score remained unchanged, a 2-year treatment decreased the initial CARS score from severe (mean ± SD: 41.34 ± 6.47) to moderate or mild autism (mean ± SD: 34.35 ± 6.25; paired t-test p<0.0001), achieving complete recovery in 17/82 children (20.7 %). Prognosis became less favorable with the finding of higher FR? autoantibody titers, positive maternal FR? autoantibodies, or FR? antibodies in both parents. Conclusions. Correction of nutritional deficiencies combined with high-dose folinic acid improved outcome for autism, although the trend of a poor prognosis due to maternal FR? antibodies or FR? antibodies in both parents may warrant folinic acid intervention before conception and during pregnancy. En ligne : https://doi.org/10.1155/2019/7486431 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=402

AMBRA1, Autophagy, and the Extreme Male Brain Theory of Autism / Bernard CRESPI in Autism Research and Treatment, 2019 (2019)  

Public ISBD [article]  inAutism Research and Treatment > 2019 (2019) . - 6 p. Titre : AMBRA1, Autophagy, and the Extreme Male Brain Theory of Autism Type de document : Texte imprimé et/ou numérique Auteurs : Bernard CRESPI, Auteur ; Silven READ, Auteur ; Amy LY, Auteur ; Peter HURD, Auteur Année de publication : 2019 Article en page(s) : 6 p. Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : The extreme male brain theory of autism posits that its male bias is mediated by exaggeration of male-biased sex differences inthe expression of autism-associated traits found in typical populations. 'e theory is supported by extensive phenotypicevidence, but no genes have yet been described with properties that fit its predictions. 'e autophagy-associated geneAMBRA1 represents one of the top genome-wide “hits” in recent GWAS studies of schizophrenia, shows sex-differentialexpression, and has been linked with autism risk and traits in humans and mice, especially or exclusively among females. Wegenotyped the AMBRA1 autism-risk SNP in a population of typical humans who were scored for the dimensional expressionof autistic and schizotypal traits. Females, but not males, homozygous for the GG genotype showed a significant increase inscore for the single trait, the Autism Quotient-Imagination subscale, that exhibits a strong, significant male bias in typicalpopulations. As such, females with this genotype resembled males for this highly sexually dimorphic, autism-associatedphenotype. 'ese findings support the extreme male brain hypothesis and indicate that sex-specific genetic effects canmediate aspects of risk for autism. En ligne : https://doi.org/10.1155/2019/1968580 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=409 [article] AMBRA1, Autophagy, and the Extreme Male Brain Theory of Autism [Texte imprimé et/ou numérique] / Bernard CRESPI, Auteur ; Silven READ, Auteur ; Amy LY, Auteur ; Peter HURD, Auteur . - 2019 . - 6 p. Langues : Anglais (eng) in Autism Research and Treatment > 2019 (2019) . - 6 p. Index. décimale : PER Périodiques Résumé : The extreme male brain theory of autism posits that its male bias is mediated by exaggeration of male-biased sex differences inthe expression of autism-associated traits found in typical populations. 'e theory is supported by extensive phenotypicevidence, but no genes have yet been described with properties that fit its predictions. 'e autophagy-associated geneAMBRA1 represents one of the top genome-wide “hits” in recent GWAS studies of schizophrenia, shows sex-differentialexpression, and has been linked with autism risk and traits in humans and mice, especially or exclusively among females. Wegenotyped the AMBRA1 autism-risk SNP in a population of typical humans who were scored for the dimensional expressionof autistic and schizotypal traits. Females, but not males, homozygous for the GG genotype showed a significant increase inscore for the single trait, the Autism Quotient-Imagination subscale, that exhibits a strong, significant male bias in typicalpopulations. As such, females with this genotype resembled males for this highly sexually dimorphic, autism-associatedphenotype. 'ese findings support the extreme male brain hypothesis and indicate that sex-specific genetic effects canmediate aspects of risk for autism. En ligne : https://doi.org/10.1155/2019/1968580 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=409