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Editorial Perspective: How to optimise frequency band neurofeedback for ADHD / Annet BLUSCHKE in Journal of Child Psychology and Psychiatry, 57-4 (April 2016)
[article]
Titre : Editorial Perspective: How to optimise frequency band neurofeedback for ADHD Type de document : Texte imprimé et/ou numérique Auteurs : Annet BLUSCHKE, Auteur ; Veit ROESSNER, Auteur ; Christian BESTE, Auteur Article en page(s) : p.457-461 Langues : Anglais (eng) Mots-clés : ADHD cognitive deficits neurofeedback treatment optimisation Index. décimale : PER Périodiques Résumé : Attention deficit/hyperactivity disorder (ADHD) is one of the most prevalent paediatric neuropsychiatric disorders and is characterised by hyperactivity, inattention and increased impulsivity. Children with ADHD are often also characterised by deficits in a variety of cognitive domains, including problems in working memory, a generally slower and more variable style of information processing and deficits in temporal processing, inhibitory functions and delay processing. Overarching executive functions like information updating, response inhibition and mental set shifting are also impaired in many, but not all, children with ADHD, demonstrating the neuropsychological heterogeneity characterising this disorder. Deficits in executive functions can persist into adulthood and have a substantial negative impact on everyday life. A variety of approaches are commonly considered for the treatment of ADHD (including pharmacological interventions, patient-centred cognitive-behavioural therapy approaches and specific teacher/parent training programmes). More recently, adding to this multimodal treatment approach, neurofeedback has grown in popularity as an intervention option for patients with ADHD. This article considers this intervention approach and the opportunities for optimising treatment for executive control dysfunctions in ADHD using theta/beta neurofeedback. En ligne : http://dx.doi.org/10.1111/jcpp.12521 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=285
in Journal of Child Psychology and Psychiatry > 57-4 (April 2016) . - p.457-461[article] Editorial Perspective: How to optimise frequency band neurofeedback for ADHD [Texte imprimé et/ou numérique] / Annet BLUSCHKE, Auteur ; Veit ROESSNER, Auteur ; Christian BESTE, Auteur . - p.457-461.
Langues : Anglais (eng)
in Journal of Child Psychology and Psychiatry > 57-4 (April 2016) . - p.457-461
Mots-clés : ADHD cognitive deficits neurofeedback treatment optimisation Index. décimale : PER Périodiques Résumé : Attention deficit/hyperactivity disorder (ADHD) is one of the most prevalent paediatric neuropsychiatric disorders and is characterised by hyperactivity, inattention and increased impulsivity. Children with ADHD are often also characterised by deficits in a variety of cognitive domains, including problems in working memory, a generally slower and more variable style of information processing and deficits in temporal processing, inhibitory functions and delay processing. Overarching executive functions like information updating, response inhibition and mental set shifting are also impaired in many, but not all, children with ADHD, demonstrating the neuropsychological heterogeneity characterising this disorder. Deficits in executive functions can persist into adulthood and have a substantial negative impact on everyday life. A variety of approaches are commonly considered for the treatment of ADHD (including pharmacological interventions, patient-centred cognitive-behavioural therapy approaches and specific teacher/parent training programmes). More recently, adding to this multimodal treatment approach, neurofeedback has grown in popularity as an intervention option for patients with ADHD. This article considers this intervention approach and the opportunities for optimising treatment for executive control dysfunctions in ADHD using theta/beta neurofeedback. En ligne : http://dx.doi.org/10.1111/jcpp.12521 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=285 Generation of a Novel Rat Model of Angelman Syndrome with a Complete Ube3a Gene Deletion / Andie DODGE in Autism Research, 13-3 (March 2020)
[article]
Titre : Generation of a Novel Rat Model of Angelman Syndrome with a Complete Ube3a Gene Deletion Type de document : Texte imprimé et/ou numérique Auteurs : Andie DODGE, Auteur ; Melinda M. PETERS, Auteur ; Hayden E. GREENE, Auteur ; Clifton DIETRICK, Auteur ; Robert BOTELHO, Auteur ; Diana CHUNG, Auteur ; Jonathan WILLMAN, Auteur ; Austin W NENNINGER, Auteur ; Stephanie CIARLONE, Auteur ; Siddharth G. KAMATH, Auteur ; Pavel HOUDEK, Auteur ; Alena SUMOVA, Auteur ; Anne E. ANDERSON, Auteur ; Scott V. DINDOT, Auteur ; Elizabeth L. BERG, Auteur ; Henriette O'GEEN, Auteur ; David J. SEGAL, Auteur ; Jill L. SILVERMAN, Auteur ; Edwin J. WEEBER, Auteur ; Kevin R. NASH, Auteur Article en page(s) : p.397-409 Langues : Anglais (eng) Mots-clés : Angelman syndrome E6ap Ube3a cognitive deficits rat model Index. décimale : PER Périodiques Résumé : Angelman syndrome (AS) is a rare genetic disorder characterized by severe intellectual disability, seizures, lack of speech, and ataxia. The gene responsible for AS was identified as Ube3a and it encodes for E6AP, an E3 ubiquitin ligase. Currently, there is very little known about E6AP's mechanism of action in vivo or how the lack of this protein in neurons may contribute to the AS phenotype. Elucidating the mechanistic action of E6AP would enhance our understanding of AS and drive current research into new avenues that could lead to novel therapeutic approaches that target E6AP's various functions. To facilitate the study of AS, we have generated a novel rat model in which we deleted the rat Ube3a gene using CRISPR. The AS rat phenotypically mirrors human AS with loss of Ube3a expression in the brain and deficits in motor coordination as well as learning and memory. This model offers a new avenue for the study of AS. Autism Res 2020, 13: 397-409. (c) 2020 International Society for Autism Research,Wiley Periodicals, Inc. LAY SUMMARY: Angelman syndrome (AS) is a rare genetic disorder characterized by severe intellectual disability, seizures, difficulty speaking, and ataxia. The gene responsible for AS was identified as UBE3A, yet very little is known about its function in vivo or how the lack of this protein in neurons may contribute to the AS phenotype. To facilitate the study of AS, we have generated a novel rat model in which we deleted the rat Ube3a gene using CRISPR. The AS rat mirrors human AS with loss of Ube3a expression in the brain and deficits in motor coordination as well as learning and memory. This model offers a new avenue for the study of AS. En ligne : http://dx.doi.org/10.1002/aur.2267 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=421
in Autism Research > 13-3 (March 2020) . - p.397-409[article] Generation of a Novel Rat Model of Angelman Syndrome with a Complete Ube3a Gene Deletion [Texte imprimé et/ou numérique] / Andie DODGE, Auteur ; Melinda M. PETERS, Auteur ; Hayden E. GREENE, Auteur ; Clifton DIETRICK, Auteur ; Robert BOTELHO, Auteur ; Diana CHUNG, Auteur ; Jonathan WILLMAN, Auteur ; Austin W NENNINGER, Auteur ; Stephanie CIARLONE, Auteur ; Siddharth G. KAMATH, Auteur ; Pavel HOUDEK, Auteur ; Alena SUMOVA, Auteur ; Anne E. ANDERSON, Auteur ; Scott V. DINDOT, Auteur ; Elizabeth L. BERG, Auteur ; Henriette O'GEEN, Auteur ; David J. SEGAL, Auteur ; Jill L. SILVERMAN, Auteur ; Edwin J. WEEBER, Auteur ; Kevin R. NASH, Auteur . - p.397-409.
Langues : Anglais (eng)
in Autism Research > 13-3 (March 2020) . - p.397-409
Mots-clés : Angelman syndrome E6ap Ube3a cognitive deficits rat model Index. décimale : PER Périodiques Résumé : Angelman syndrome (AS) is a rare genetic disorder characterized by severe intellectual disability, seizures, lack of speech, and ataxia. The gene responsible for AS was identified as Ube3a and it encodes for E6AP, an E3 ubiquitin ligase. Currently, there is very little known about E6AP's mechanism of action in vivo or how the lack of this protein in neurons may contribute to the AS phenotype. Elucidating the mechanistic action of E6AP would enhance our understanding of AS and drive current research into new avenues that could lead to novel therapeutic approaches that target E6AP's various functions. To facilitate the study of AS, we have generated a novel rat model in which we deleted the rat Ube3a gene using CRISPR. The AS rat phenotypically mirrors human AS with loss of Ube3a expression in the brain and deficits in motor coordination as well as learning and memory. This model offers a new avenue for the study of AS. Autism Res 2020, 13: 397-409. (c) 2020 International Society for Autism Research,Wiley Periodicals, Inc. LAY SUMMARY: Angelman syndrome (AS) is a rare genetic disorder characterized by severe intellectual disability, seizures, difficulty speaking, and ataxia. The gene responsible for AS was identified as UBE3A, yet very little is known about its function in vivo or how the lack of this protein in neurons may contribute to the AS phenotype. To facilitate the study of AS, we have generated a novel rat model in which we deleted the rat Ube3a gene using CRISPR. The AS rat mirrors human AS with loss of Ube3a expression in the brain and deficits in motor coordination as well as learning and memory. This model offers a new avenue for the study of AS. En ligne : http://dx.doi.org/10.1002/aur.2267 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=421