- <Centre d'Information et de documentation du CRA Rhône-Alpes
- CRA
- Informations pratiques
-
Adresse
Centre d'information et de documentation
Horaires
du CRA Rhône-Alpes
Centre Hospitalier le Vinatier
bât 211
95, Bd Pinel
69678 Bron CedexLundi au Vendredi
Contact
9h00-12h00 13h30-16h00Tél: +33(0)4 37 91 54 65
Mail
Fax: +33(0)4 37 91 54 37
-
Adresse
Autism Research . 1-3Paru le : 01/06/2008 |
[n° ou bulletin]
[n° ou bulletin]
1-3 - June 2008 [Texte imprimé et/ou numérique] . - 2008.
|
Exemplaires (1)
Code-barres | Cote | Support | Localisation | Section | Disponibilité |
---|---|---|---|---|---|
PER0000403 | PER ARI | Périodique | Centre d'Information et de Documentation du CRA Rhône-Alpes | PER - Périodiques | Exclu du prêt |
Dépouillements
Ajouter le résultat dans votre panier
[article]
Titre : Autism as a Global Challenge Type de document : Texte imprimé et/ou numérique Auteurs : Anthony J. BAILEY, Auteur ; Valerie KARR, Auteur Année de publication : 2008 Article en page(s) : p.145-146 Langues : Anglais (eng) Index. décimale : PER Périodiques En ligne : http://dx.doi.org/10.1002/aur.28 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=931
in Autism Research > 1-3 (June 2008) . - p.145-146[article] Autism as a Global Challenge [Texte imprimé et/ou numérique] / Anthony J. BAILEY, Auteur ; Valerie KARR, Auteur . - 2008 . - p.145-146.
Langues : Anglais (eng)
in Autism Research > 1-3 (June 2008) . - p.145-146
Index. décimale : PER Périodiques En ligne : http://dx.doi.org/10.1002/aur.28 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=931 Minimal aberrant behavioral phenotypes of neuroligin-3 R451C knockin mice / Kathryn K. CHADMAN in Autism Research, 1-3 (June 2008)
[article]
Titre : Minimal aberrant behavioral phenotypes of neuroligin-3 R451C knockin mice Type de document : Texte imprimé et/ou numérique Auteurs : Kathryn K. CHADMAN, Auteur ; Nathaniel HEINTZ, Auteur ; Shiaoching GONG, Auteur ; Maria Luisa SCATTONI, Auteur ; Sarah E. BOLTUCK, Auteur ; Shruti U. GANDHY, Auteur ; Jacqueline N. CRAWLEY, Auteur Année de publication : 2008 Article en page(s) : p.147-158 Langues : Anglais (eng) Mots-clés : autism mouse-model neuroligin behavior-phenotyping social-behavior Index. décimale : PER Périodiques Résumé : Neuroligin-3 is a member of the class of cell adhesion proteins that mediate synapse development and have been implicated in autism. Mice with the human R451C mutation (NL3), identical to the point mutation found in two brothers with autism spectrum disorders, were generated and phenotyped in multiple behavioral assays with face validity to the diagnostic symptoms of autism. No differences between NL3 and their wildtype (WT) littermate controls were detected on measures of juvenile reciprocal social interaction, adult social approach, cognitive abilities, and resistance to change in a spatial habit, findings which were replicated in several cohorts of males and females. Physical and procedural abilities were similar across genotypes on measures of general health, sensory abilities, sensorimotor gating, motor functions, and anxiety-related traits. Minor developmental differences were detected between NL3 and WT, including slightly different rates of somatic growth, slower righting reflexes at postnatal days 2-6, faster homing reflexes in females, and less vocalizations on postnatal day 8 in males. Significant differences in NL3 adults included somewhat longer latencies to fall from the rotarod, less vertical activity in the open field, and less acoustic startle to high decibel tones. The humanized R451C mutation in mice did not result in apparent autism-like phenotypes, but produced detectable functional consequences that may be interpreted in terms of physical development and/or reduced sensitivity to stimuli. En ligne : http://dx.doi.org/10.1002/aur.22 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=931
in Autism Research > 1-3 (June 2008) . - p.147-158[article] Minimal aberrant behavioral phenotypes of neuroligin-3 R451C knockin mice [Texte imprimé et/ou numérique] / Kathryn K. CHADMAN, Auteur ; Nathaniel HEINTZ, Auteur ; Shiaoching GONG, Auteur ; Maria Luisa SCATTONI, Auteur ; Sarah E. BOLTUCK, Auteur ; Shruti U. GANDHY, Auteur ; Jacqueline N. CRAWLEY, Auteur . - 2008 . - p.147-158.
Langues : Anglais (eng)
in Autism Research > 1-3 (June 2008) . - p.147-158
Mots-clés : autism mouse-model neuroligin behavior-phenotyping social-behavior Index. décimale : PER Périodiques Résumé : Neuroligin-3 is a member of the class of cell adhesion proteins that mediate synapse development and have been implicated in autism. Mice with the human R451C mutation (NL3), identical to the point mutation found in two brothers with autism spectrum disorders, were generated and phenotyped in multiple behavioral assays with face validity to the diagnostic symptoms of autism. No differences between NL3 and their wildtype (WT) littermate controls were detected on measures of juvenile reciprocal social interaction, adult social approach, cognitive abilities, and resistance to change in a spatial habit, findings which were replicated in several cohorts of males and females. Physical and procedural abilities were similar across genotypes on measures of general health, sensory abilities, sensorimotor gating, motor functions, and anxiety-related traits. Minor developmental differences were detected between NL3 and WT, including slightly different rates of somatic growth, slower righting reflexes at postnatal days 2-6, faster homing reflexes in females, and less vocalizations on postnatal day 8 in males. Significant differences in NL3 adults included somewhat longer latencies to fall from the rotarod, less vertical activity in the open field, and less acoustic startle to high decibel tones. The humanized R451C mutation in mice did not result in apparent autism-like phenotypes, but produced detectable functional consequences that may be interpreted in terms of physical development and/or reduced sensitivity to stimuli. En ligne : http://dx.doi.org/10.1002/aur.22 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=931 Genetic evidence implicating multiple genes in the MET receptor tyrosine kinase pathway in autism spectrum disorder / Daniel B. CAMPBELL in Autism Research, 1-3 (June 2008)
[article]
Titre : Genetic evidence implicating multiple genes in the MET receptor tyrosine kinase pathway in autism spectrum disorder Type de document : Texte imprimé et/ou numérique Auteurs : Daniel B. CAMPBELL, Auteur ; Antonio M. PERSICO, Auteur ; James S. SUTCLIFFE, Auteur ; Chun LI, Auteur ; Pat LEVITT, Auteur Année de publication : 2008 Article en page(s) : p.159-168 Langues : Anglais (eng) Mots-clés : genetic association plasminogen PLAUR uPAR SERPINE1 brain cerebral-cortex Index. décimale : PER Périodiques Résumé : A functional promoter variant of the gene encoding the MET receptor tyrosine kinase alters SP1 and SUB1 transcription factor binding, and is associated with autism spectrum disorder (ASD). Recent analyses of postmortem cerebral cortex from ASD patients revealed altered expression of MET protein and three transcripts encoding proteins that regulate MET signaling, hepatocyte growth factor (HGF), urokinase plasminogen activator receptor (PLAUR) and plasminogen activator inhibitor-1 (SERPINE1). To address potential risk conferred by multiple genes in the MET signaling pathway, we screened all exons and 5 promoter regions for variants in the five genes encoding proteins that regulate MET expression and activity. Identified variants were genotyped in 664 families (2,712 individuals including 1,228 with ASD) and 312 unrelated controls. Replicating our initial findings, family-based association test (FBAT) analyses demonstrated that the MET promoter variant rs1858830 C allele was associated with ASD in 101 new families (P=0.033). Two other genes in the MET signaling pathway also may confer risk. A haplotype of the SERPINE1 gene exhibited significant association. In addition, the PLAUR promoter variant rs344781 T allele was associated with ASD by both FBAT (P=0.006) and case-control analyses (P=0.007). The PLAUR promoter rs344781 relative risk was 1.93 (95% confidence interval [CI]: 1.12-3.31) for genotype TT and 2.42 (95% CI: 1.38-4.25) for genotype CT compared to genotype CC. Gene-gene interaction analyses suggested a significant interaction between MET and PLAUR. These data further support our hypothesis that genetic susceptibility impacting multiple components of the MET signaling pathway contributes to ASD risk. En ligne : http://dx.doi.org/10.1002/aur.27 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=931
in Autism Research > 1-3 (June 2008) . - p.159-168[article] Genetic evidence implicating multiple genes in the MET receptor tyrosine kinase pathway in autism spectrum disorder [Texte imprimé et/ou numérique] / Daniel B. CAMPBELL, Auteur ; Antonio M. PERSICO, Auteur ; James S. SUTCLIFFE, Auteur ; Chun LI, Auteur ; Pat LEVITT, Auteur . - 2008 . - p.159-168.
Langues : Anglais (eng)
in Autism Research > 1-3 (June 2008) . - p.159-168
Mots-clés : genetic association plasminogen PLAUR uPAR SERPINE1 brain cerebral-cortex Index. décimale : PER Périodiques Résumé : A functional promoter variant of the gene encoding the MET receptor tyrosine kinase alters SP1 and SUB1 transcription factor binding, and is associated with autism spectrum disorder (ASD). Recent analyses of postmortem cerebral cortex from ASD patients revealed altered expression of MET protein and three transcripts encoding proteins that regulate MET signaling, hepatocyte growth factor (HGF), urokinase plasminogen activator receptor (PLAUR) and plasminogen activator inhibitor-1 (SERPINE1). To address potential risk conferred by multiple genes in the MET signaling pathway, we screened all exons and 5 promoter regions for variants in the five genes encoding proteins that regulate MET expression and activity. Identified variants were genotyped in 664 families (2,712 individuals including 1,228 with ASD) and 312 unrelated controls. Replicating our initial findings, family-based association test (FBAT) analyses demonstrated that the MET promoter variant rs1858830 C allele was associated with ASD in 101 new families (P=0.033). Two other genes in the MET signaling pathway also may confer risk. A haplotype of the SERPINE1 gene exhibited significant association. In addition, the PLAUR promoter variant rs344781 T allele was associated with ASD by both FBAT (P=0.006) and case-control analyses (P=0.007). The PLAUR promoter rs344781 relative risk was 1.93 (95% confidence interval [CI]: 1.12-3.31) for genotype TT and 2.42 (95% CI: 1.38-4.25) for genotype CT compared to genotype CC. Gene-gene interaction analyses suggested a significant interaction between MET and PLAUR. These data further support our hypothesis that genetic susceptibility impacting multiple components of the MET signaling pathway contributes to ASD risk. En ligne : http://dx.doi.org/10.1002/aur.27 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=931 MECP2 promoter methylation and X chromosome inactivation in autism / Raman P. NAGARAJAN in Autism Research, 1-3 (June 2008)
[article]
Titre : MECP2 promoter methylation and X chromosome inactivation in autism Type de document : Texte imprimé et/ou numérique Auteurs : Raman P. NAGARAJAN, Auteur ; Irva HERTZ-PICCIOTTO, Auteur ; Wendy P. ROBINSON, Auteur ; Ruby JIANG, Auteur ; Susan E. SWANBERG, Auteur ; Dag H. YASUI, Auteur ; Michelle MARTIN, Auteur ; Katherine A. PATZEL, Auteur ; Janine M. LASALLE, Auteur ; Judy VAN DE WATER, Auteur ; Isaac N. PESSAH, Auteur ; David J. HANSEN, Auteur Année de publication : 2008 Article en page(s) : p.169-178 Langues : Anglais (eng) Mots-clés : epigenetics X-chromosome-inactivation MECP2 postmortem-brain Index. décimale : PER Périodiques Résumé : Epigenetic mechanisms have been proposed to play a role in the etiology of autism. This hypothesis is supported by the discovery of increased MECP2 promoter methylation associated with decreased MeCP2 protein expression in autism male brain. To further understand the influence of female X chromosome inactivation (XCI) and neighboring methylation patterns on aberrant MECP2 promoter methylation in autism, multiple methylation analyses were performed on brain and blood samples from individuals with autism. Bisulfite sequencing analyses of a region 0.6 kb upstream of MECP2 in brain DNA samples revealed an abrupt transition from a highly methylated region in both sexes to a region unmethylated in males and subject to XCI in females. Chromatin immunoprecipitation analysis demonstrated that the CCCTC-binding factor (CTCF) is bound to this transition region in neuronal cells, consistent with a chromatin boundary at the methylation transition. Male autism brain DNA samples displayed a slight increase in methylation in this transition region, suggesting a possible aberrant spreading of methylation into the MECP2 promoter in autism males across this boundary element. In addition, autistic female brain DNA samples showed evidence for aberrant MECP2 promoter methylation as an increase in the number of bisulfite sequenced clones with undefined XCI status for MECP2 but not androgen receptor (AR). To further investigate the specificity of MECP2 methylation alterations in autism, blood DNA samples from females and mothers of males with autism were also examined for XCI skewing at AR, but no significant increase in XCI skewing was observed compared to controls. These results suggest that the aberrant MECP2 methylation in autism brain DNA samples is due to locus-specific rather than global X chromosome methylation changes. En ligne : http://dx.doi.org/10.1002/aur.24 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=931
in Autism Research > 1-3 (June 2008) . - p.169-178[article] MECP2 promoter methylation and X chromosome inactivation in autism [Texte imprimé et/ou numérique] / Raman P. NAGARAJAN, Auteur ; Irva HERTZ-PICCIOTTO, Auteur ; Wendy P. ROBINSON, Auteur ; Ruby JIANG, Auteur ; Susan E. SWANBERG, Auteur ; Dag H. YASUI, Auteur ; Michelle MARTIN, Auteur ; Katherine A. PATZEL, Auteur ; Janine M. LASALLE, Auteur ; Judy VAN DE WATER, Auteur ; Isaac N. PESSAH, Auteur ; David J. HANSEN, Auteur . - 2008 . - p.169-178.
Langues : Anglais (eng)
in Autism Research > 1-3 (June 2008) . - p.169-178
Mots-clés : epigenetics X-chromosome-inactivation MECP2 postmortem-brain Index. décimale : PER Périodiques Résumé : Epigenetic mechanisms have been proposed to play a role in the etiology of autism. This hypothesis is supported by the discovery of increased MECP2 promoter methylation associated with decreased MeCP2 protein expression in autism male brain. To further understand the influence of female X chromosome inactivation (XCI) and neighboring methylation patterns on aberrant MECP2 promoter methylation in autism, multiple methylation analyses were performed on brain and blood samples from individuals with autism. Bisulfite sequencing analyses of a region 0.6 kb upstream of MECP2 in brain DNA samples revealed an abrupt transition from a highly methylated region in both sexes to a region unmethylated in males and subject to XCI in females. Chromatin immunoprecipitation analysis demonstrated that the CCCTC-binding factor (CTCF) is bound to this transition region in neuronal cells, consistent with a chromatin boundary at the methylation transition. Male autism brain DNA samples displayed a slight increase in methylation in this transition region, suggesting a possible aberrant spreading of methylation into the MECP2 promoter in autism males across this boundary element. In addition, autistic female brain DNA samples showed evidence for aberrant MECP2 promoter methylation as an increase in the number of bisulfite sequenced clones with undefined XCI status for MECP2 but not androgen receptor (AR). To further investigate the specificity of MECP2 methylation alterations in autism, blood DNA samples from females and mothers of males with autism were also examined for XCI skewing at AR, but no significant increase in XCI skewing was observed compared to controls. These results suggest that the aberrant MECP2 methylation in autism brain DNA samples is due to locus-specific rather than global X chromosome methylation changes. En ligne : http://dx.doi.org/10.1002/aur.24 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=931 Detecting changes in naturalistic scenes: contextual inconsistency does not influence spontaneous attention in high-functioning people with autism spectrum disorder / Eva LOTH in Autism Research, 1-3 (June 2008)
[article]
Titre : Detecting changes in naturalistic scenes: contextual inconsistency does not influence spontaneous attention in high-functioning people with autism spectrum disorder Type de document : Texte imprimé et/ou numérique Auteurs : Eva LOTH, Auteur ; Francesca HAPPE, Auteur ; Juan-Carlos GOMEZ, Auteur Année de publication : 2008 Article en page(s) : p.179-188 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Individuals with autism spectrum disorders (ASD) are often reported to be good at detecting minute changes in the environment. This study tested two factors in this phenomenon; detail-focus and reduced top-down influence of scene-schema expectations on spontaneous attention to visual scene elements. Using a change blindness paradigm, adults with ASD and matched typically developing (TD) adults were presented with images of naturalistic scenes (e.g., living room). Scene changes involved three types of object substitution: an object was replaced with (i) an unexpected scene-unrelated object, (ii) a scene-related object of a different basic-level category, (iii) or a different exemplar of the original object category. Top-down effects of scene-schema expectations should render scene-unrelated (i) substitutions easiest to recognize; detail focus should increase detection of exemplar changes. The TD group showed the expected condition effects, detecting scene-unrelated substitutions significantly better than both types of scene-related changes. By contrast, the ASD group showed no condition effect, and was only significantly slower and less accurate than the TD group in detecting scene-unrelated objects. These findings suggest reduced influence of schematic expectations on spontaneous attention in individuals with ASD. Together with other factors, this may contribute to the tendency to notice irrelevant changes in the environment. En ligne : http://dx.doi.org/10.1002/aur.19 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=931
in Autism Research > 1-3 (June 2008) . - p.179-188[article] Detecting changes in naturalistic scenes: contextual inconsistency does not influence spontaneous attention in high-functioning people with autism spectrum disorder [Texte imprimé et/ou numérique] / Eva LOTH, Auteur ; Francesca HAPPE, Auteur ; Juan-Carlos GOMEZ, Auteur . - 2008 . - p.179-188.
Langues : Anglais (eng)
in Autism Research > 1-3 (June 2008) . - p.179-188
Index. décimale : PER Périodiques Résumé : Individuals with autism spectrum disorders (ASD) are often reported to be good at detecting minute changes in the environment. This study tested two factors in this phenomenon; detail-focus and reduced top-down influence of scene-schema expectations on spontaneous attention to visual scene elements. Using a change blindness paradigm, adults with ASD and matched typically developing (TD) adults were presented with images of naturalistic scenes (e.g., living room). Scene changes involved three types of object substitution: an object was replaced with (i) an unexpected scene-unrelated object, (ii) a scene-related object of a different basic-level category, (iii) or a different exemplar of the original object category. Top-down effects of scene-schema expectations should render scene-unrelated (i) substitutions easiest to recognize; detail focus should increase detection of exemplar changes. The TD group showed the expected condition effects, detecting scene-unrelated substitutions significantly better than both types of scene-related changes. By contrast, the ASD group showed no condition effect, and was only significantly slower and less accurate than the TD group in detecting scene-unrelated objects. These findings suggest reduced influence of schematic expectations on spontaneous attention in individuals with ASD. Together with other factors, this may contribute to the tendency to notice irrelevant changes in the environment. En ligne : http://dx.doi.org/10.1002/aur.19 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=931 Mitochondrial aspartate/glutamate carrier SLC25A12 gene is associated with autism / Joni A. TURUNEN in Autism Research, 1-3 (June 2008)
[article]
Titre : Mitochondrial aspartate/glutamate carrier SLC25A12 gene is associated with autism Type de document : Texte imprimé et/ou numérique Auteurs : Joni A. TURUNEN, Auteur ; Karola REHNSTROM, Auteur ; Helena KILPINEN, Auteur ; Mikko KUOKKANEN, Auteur ; Elli KEMPAS, Auteur ; Tero YLISAUKKO-OJA, Auteur Année de publication : 2008 Article en page(s) : p.189-192 Langues : Anglais (eng) Mots-clés : autism Asperger-syndrome SLC25A12 association SNP Index. décimale : PER Périodiques Résumé : Two single nucleotide polymorphisms (SNP) within Mitochondrial Aspartate/Glutamate Carrier SLC25A12 gene have recently shown to be strongly associated with autism. Here, we attempted to replicate this finding in two separate Finnish samples with autism spectrum disorders. Family-based association analysis of two SNPs, rs2056202 and rs2292813, previously shown to be associated with autism was performed in two samples with different phenotypic characteristics. The samples included 97 families with strictly defined autism and 29 extended families with Asperger syndrome (AS). We detected association at rs2292813 (FBAT, P=0.0018) in the Finnish autism sample. In, addition other family-based analysis methods supported this finding. By contrast, analysis of the AS sample yielded no evidence for association. This study shows further support that genetic variants within SLC25A12 gene contribute to the etiology of autism. En ligne : http://dx.doi.org/10.1002/aur.25 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=931
in Autism Research > 1-3 (June 2008) . - p.189-192[article] Mitochondrial aspartate/glutamate carrier SLC25A12 gene is associated with autism [Texte imprimé et/ou numérique] / Joni A. TURUNEN, Auteur ; Karola REHNSTROM, Auteur ; Helena KILPINEN, Auteur ; Mikko KUOKKANEN, Auteur ; Elli KEMPAS, Auteur ; Tero YLISAUKKO-OJA, Auteur . - 2008 . - p.189-192.
Langues : Anglais (eng)
in Autism Research > 1-3 (June 2008) . - p.189-192
Mots-clés : autism Asperger-syndrome SLC25A12 association SNP Index. décimale : PER Périodiques Résumé : Two single nucleotide polymorphisms (SNP) within Mitochondrial Aspartate/Glutamate Carrier SLC25A12 gene have recently shown to be strongly associated with autism. Here, we attempted to replicate this finding in two separate Finnish samples with autism spectrum disorders. Family-based association analysis of two SNPs, rs2056202 and rs2292813, previously shown to be associated with autism was performed in two samples with different phenotypic characteristics. The samples included 97 families with strictly defined autism and 29 extended families with Asperger syndrome (AS). We detected association at rs2292813 (FBAT, P=0.0018) in the Finnish autism sample. In, addition other family-based analysis methods supported this finding. By contrast, analysis of the AS sample yielded no evidence for association. This study shows further support that genetic variants within SLC25A12 gene contribute to the etiology of autism. En ligne : http://dx.doi.org/10.1002/aur.25 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=931 Overrepresentation of mood and anxiety disorders in adults with autism and their first-degree relatives: what does it mean? / Carla A. MAZEFSKY in Autism Research, 1-3 (June 2008)
[article]
Titre : Overrepresentation of mood and anxiety disorders in adults with autism and their first-degree relatives: what does it mean? Type de document : Texte imprimé et/ou numérique Auteurs : Carla A. MAZEFSKY, Auteur ; Janet E. LAINHART, Auteur ; S. E. FOLSTEIN, Auteur Année de publication : 2008 Article en page(s) : p.193-197 Langues : Anglais (eng) Mots-clés : familial-aggregation affective-disorders family-history autism co-morbidity Index. décimale : PER Périodiques Résumé : Research indicates that relatives of individuals with autism have higher rates of affective disorders than both the general population and families of children with other developmental disabilities. In addition, individuals with autism have high rates of co-morbid mood and anxiety disorders. This study sought to identify possible reasons for these previous findings by documenting the presence of affective disorders in both probands (the individuals with autism) and their family members. A sub-sample of 17 adults with autism and their first-degree relatives from the Baltimore Family Study of Autism completed a structured psychiatric interview. The results indicated that the rates of mood and anxiety disorders were 35 and 77%, respectively, for probands, and these disorders were present in at least one first-degree relative at rates of 71 and 29%, respectively. Exploring patterns within families revealed that 80% of probands with a mother who had a mood disorder history also had a mood disorder themselves, compared to only 16% of probands whose mothers did not have a mood disorder history. The results must be considered preliminary given the small sample size. Replicating these findings in a larger sample would help clarify whether a true increased risk of mood disorder exists, which would have potential implications for prevention efforts and understanding possible genetic mechanisms. En ligne : http://dx.doi.org/10.1002/aur.23 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=931
in Autism Research > 1-3 (June 2008) . - p.193-197[article] Overrepresentation of mood and anxiety disorders in adults with autism and their first-degree relatives: what does it mean? [Texte imprimé et/ou numérique] / Carla A. MAZEFSKY, Auteur ; Janet E. LAINHART, Auteur ; S. E. FOLSTEIN, Auteur . - 2008 . - p.193-197.
Langues : Anglais (eng)
in Autism Research > 1-3 (June 2008) . - p.193-197
Mots-clés : familial-aggregation affective-disorders family-history autism co-morbidity Index. décimale : PER Périodiques Résumé : Research indicates that relatives of individuals with autism have higher rates of affective disorders than both the general population and families of children with other developmental disabilities. In addition, individuals with autism have high rates of co-morbid mood and anxiety disorders. This study sought to identify possible reasons for these previous findings by documenting the presence of affective disorders in both probands (the individuals with autism) and their family members. A sub-sample of 17 adults with autism and their first-degree relatives from the Baltimore Family Study of Autism completed a structured psychiatric interview. The results indicated that the rates of mood and anxiety disorders were 35 and 77%, respectively, for probands, and these disorders were present in at least one first-degree relative at rates of 71 and 29%, respectively. Exploring patterns within families revealed that 80% of probands with a mother who had a mood disorder history also had a mood disorder themselves, compared to only 16% of probands whose mothers did not have a mood disorder history. The results must be considered preliminary given the small sample size. Replicating these findings in a larger sample would help clarify whether a true increased risk of mood disorder exists, which would have potential implications for prevention efforts and understanding possible genetic mechanisms. En ligne : http://dx.doi.org/10.1002/aur.23 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=931
[article]
Titre : Literature Review Type de document : Texte imprimé et/ou numérique Auteurs : Edwin H. Jr COOK, Auteur Année de publication : 2008 Article en page(s) : p.198-200 Langues : Anglais (eng) Index. décimale : PER Périodiques En ligne : http://dx.doi.org/10.1002/aur.26 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=932
in Autism Research > 1-3 (June 2008) . - p.198-200[article] Literature Review [Texte imprimé et/ou numérique] / Edwin H. Jr COOK, Auteur . - 2008 . - p.198-200.
Langues : Anglais (eng)
in Autism Research > 1-3 (June 2008) . - p.198-200
Index. décimale : PER Périodiques En ligne : http://dx.doi.org/10.1002/aur.26 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=932
[article]
Titre : Lay abstracts Type de document : Texte imprimé et/ou numérique Année de publication : 2008 Article en page(s) : p.201-203 Langues : Anglais (eng) Index. décimale : PER Périodiques En ligne : http://dx.doi.org/10.1002/aur.29 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=932
in Autism Research > 1-3 (June 2008) . - p.201-203[article] Lay abstracts [Texte imprimé et/ou numérique] . - 2008 . - p.201-203.
Langues : Anglais (eng)
in Autism Research > 1-3 (June 2008) . - p.201-203
Index. décimale : PER Périodiques En ligne : http://dx.doi.org/10.1002/aur.29 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=932
[article]
Titre : International Society for Autism Research News Type de document : Texte imprimé et/ou numérique Année de publication : 2008 Article en page(s) : p.204 Langues : Anglais (eng) Index. décimale : PER Périodiques En ligne : http://dx.doi.org/10.1002/aur.31 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=932
in Autism Research > 1-3 (June 2008) . - p.204[article] International Society for Autism Research News [Texte imprimé et/ou numérique] . - 2008 . - p.204.
Langues : Anglais (eng)
in Autism Research > 1-3 (June 2008) . - p.204
Index. décimale : PER Périodiques En ligne : http://dx.doi.org/10.1002/aur.31 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=932