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Male predominance in autism: neuroendocrine influences on arousal and social anxiety / Donald W. PFAFF in Autism Research, 4-3 (June 2011)
[article]
Titre : Male predominance in autism: neuroendocrine influences on arousal and social anxiety Type de document : Texte imprimé et/ou numérique Auteurs : Donald W. PFAFF, Auteur ; Isabelle RAPIN, Auteur ; Sylvie GOLDMAN, Auteur Année de publication : 2011 Article en page(s) : p.163-176 Langues : Anglais (eng) Mots-clés : behavioral analysis of animal models developmental neurobiology sex differences testosterone androgen receptor Index. décimale : PER Périodiques Résumé : We offer a neurobiologic theory based on animal work that helps account for the conspicuous male predominance in autism spectrum disorders (ASD). In young male animals, testosterone (TST) binds to androgen receptors (AR) in brainstem neurons responsible for enhancing brain arousal. As a consequence, arousal-related neurotransmitters bombard the amygdala hypersensitized by TST acting though AR. Arousal-related inputs are known to prime amygdaloid mechanisms for fear and anxiety, with resultant social avoidance. We hypothesize that similar mechanisms contribute to autism's male predominance and to its defining impaired social skills. The theory rests on two key interacting factors: the molecular effects of TST in genetically vulnerable boys in combination with environmental stresses they experienced in utero, neonatally, or during the first years. We postulate that higher TST levels and, therefore, higher amounts of arousal-related inputs to the amygdala sensitize these genetically vulnerable male infants to very early stresses. In sharp contrast to boys, girls not only do not have high levels of TST-facilitated arousal-causing inputs to the amygdala but they also enjoy the protection afforded by estrogenic hormones, oxytocin, and the oxytocin receptor. This theory suggests that novel technologies applied to the molecular endocrinology of TST's actions through AR will offer new avenues of enquiry into ASD. Since the high male preponderance in autism is important yet understudied, we offer our theory, which is based on detailed neurobehavioral research with animals, to stimulate basic and clinical research in animals and humans and hopefully help develop novel more effective medical treatments for autism. En ligne : http://dx.doi.org/10.1002/aur.191 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=127
in Autism Research > 4-3 (June 2011) . - p.163-176[article] Male predominance in autism: neuroendocrine influences on arousal and social anxiety [Texte imprimé et/ou numérique] / Donald W. PFAFF, Auteur ; Isabelle RAPIN, Auteur ; Sylvie GOLDMAN, Auteur . - 2011 . - p.163-176.
Langues : Anglais (eng)
in Autism Research > 4-3 (June 2011) . - p.163-176
Mots-clés : behavioral analysis of animal models developmental neurobiology sex differences testosterone androgen receptor Index. décimale : PER Périodiques Résumé : We offer a neurobiologic theory based on animal work that helps account for the conspicuous male predominance in autism spectrum disorders (ASD). In young male animals, testosterone (TST) binds to androgen receptors (AR) in brainstem neurons responsible for enhancing brain arousal. As a consequence, arousal-related neurotransmitters bombard the amygdala hypersensitized by TST acting though AR. Arousal-related inputs are known to prime amygdaloid mechanisms for fear and anxiety, with resultant social avoidance. We hypothesize that similar mechanisms contribute to autism's male predominance and to its defining impaired social skills. The theory rests on two key interacting factors: the molecular effects of TST in genetically vulnerable boys in combination with environmental stresses they experienced in utero, neonatally, or during the first years. We postulate that higher TST levels and, therefore, higher amounts of arousal-related inputs to the amygdala sensitize these genetically vulnerable male infants to very early stresses. In sharp contrast to boys, girls not only do not have high levels of TST-facilitated arousal-causing inputs to the amygdala but they also enjoy the protection afforded by estrogenic hormones, oxytocin, and the oxytocin receptor. This theory suggests that novel technologies applied to the molecular endocrinology of TST's actions through AR will offer new avenues of enquiry into ASD. Since the high male preponderance in autism is important yet understudied, we offer our theory, which is based on detailed neurobehavioral research with animals, to stimulate basic and clinical research in animals and humans and hopefully help develop novel more effective medical treatments for autism. En ligne : http://dx.doi.org/10.1002/aur.191 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=127 No evidence for IL1RAPL1 involvement in selected high-risk autism pedigrees from the AGRE data set / Kristina ALLEN-BRADY in Autism Research, 4-4 (August 2011)
[article]
Titre : No evidence for IL1RAPL1 involvement in selected high-risk autism pedigrees from the AGRE data set Type de document : Texte imprimé et/ou numérique Auteurs : Kristina ALLEN-BRADY, Auteur ; Guiqing CAI, Auteur ; Dale CANNON, Auteur ; Reid ROBISON, Auteur ; William M. MCMAHON, Auteur ; Hilary H. COON, Auteur ; Joseph D. BUXBAUM, Auteur Année de publication : 2011 Article en page(s) : p.293-296 Langues : Anglais (eng) Mots-clés : behavioral analysis of animal models developmental neurobiology sex differences testosterone androgen receptor Index. décimale : PER Périodiques Résumé : Finding predisposition genes for Autism Spectrum Disorder (ASD) has proven challenging, and new methods are needed to aid the process. Using pedigree structure as a strategy to identify ASD predisposition genes, we previously performed a genome-wide linkage scan of 86 selected families from the Autism Resource Exchange (AGRE) that appeared to inherit ASD in a dominant manner. We identified a suggestive linkage peak on chromosome Xp22.11-p21.2 that encompasses the IL1RAPL1 gene, a strong candidate gene for ASD. In this follow-up study, we sequenced the coding regions of the IL1RAPL1 gene in 14 male cases representing one case from each pedigree that showed at least nominal linkage evidence on per pedigree basis to the chromosome X region. We observed no deleterious mutations or deletions in the IL1RAPL1 gene in these 14 ASD cases. A SNP was identified in exon 2 in five cases and a variant of unknown significance was identified in intron 6 in a single case. In conclusion, coding changes of the IL1RAPL1 gene do not appear to be associated with ASD in selected AGRE families with linkage evidence to the chromosome Xp22.11-p21.2 region. En ligne : http://dx.doi.org/10.1002/aur.195 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=141
in Autism Research > 4-4 (August 2011) . - p.293-296[article] No evidence for IL1RAPL1 involvement in selected high-risk autism pedigrees from the AGRE data set [Texte imprimé et/ou numérique] / Kristina ALLEN-BRADY, Auteur ; Guiqing CAI, Auteur ; Dale CANNON, Auteur ; Reid ROBISON, Auteur ; William M. MCMAHON, Auteur ; Hilary H. COON, Auteur ; Joseph D. BUXBAUM, Auteur . - 2011 . - p.293-296.
Langues : Anglais (eng)
in Autism Research > 4-4 (August 2011) . - p.293-296
Mots-clés : behavioral analysis of animal models developmental neurobiology sex differences testosterone androgen receptor Index. décimale : PER Périodiques Résumé : Finding predisposition genes for Autism Spectrum Disorder (ASD) has proven challenging, and new methods are needed to aid the process. Using pedigree structure as a strategy to identify ASD predisposition genes, we previously performed a genome-wide linkage scan of 86 selected families from the Autism Resource Exchange (AGRE) that appeared to inherit ASD in a dominant manner. We identified a suggestive linkage peak on chromosome Xp22.11-p21.2 that encompasses the IL1RAPL1 gene, a strong candidate gene for ASD. In this follow-up study, we sequenced the coding regions of the IL1RAPL1 gene in 14 male cases representing one case from each pedigree that showed at least nominal linkage evidence on per pedigree basis to the chromosome X region. We observed no deleterious mutations or deletions in the IL1RAPL1 gene in these 14 ASD cases. A SNP was identified in exon 2 in five cases and a variant of unknown significance was identified in intron 6 in a single case. In conclusion, coding changes of the IL1RAPL1 gene do not appear to be associated with ASD in selected AGRE families with linkage evidence to the chromosome Xp22.11-p21.2 region. En ligne : http://dx.doi.org/10.1002/aur.195 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=141