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Type | Page Web |
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URL | http://search.proquest.com/openview/a3f42157410e9f8bb957a05744b2c932/1?pq-origsite=gscholar |
Consulté le | 22/05/2016 à 23:05:59 |
Titre abrégé | Autism and genius |
Date d'ajout | 22/05/2016 à 23:05:59 |
Modifié le | 22/05/2016 à 23:05:59 |
Type | Page Web |
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URL | http://www.medscape.com/viewarticle/841615 |
Consulté le | 16/05/2016 à 00:07:31 |
Date d'ajout | 16/05/2016 à 00:07:31 |
Modifié le | 16/05/2016 à 00:07:31 |
Type | Article de revue |
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Auteur | T.-K. Clarke |
Auteur | M. K. Lupton |
Auteur | A. M. Fernandez-Pujals |
Auteur | J. Starr |
Auteur | G. Davies |
Auteur | S. Cox |
Auteur | A. Pattie |
Auteur | D. C. Liewald |
Auteur | L. S. Hall |
Auteur | D. J. MacIntyre |
Auteur | B. H. Smith |
Auteur | L. J. Hocking |
Auteur | S. Padmanabhan |
Auteur | P. A. Thomson |
Auteur | C. Hayward |
Auteur | N. K. Hansell |
Auteur | G. W. Montgomery |
Auteur | S. E. Medland |
Auteur | N. G. Martin |
Auteur | M. J. Wright |
Auteur | D. J. Porteous |
Auteur | I. J. Deary |
Auteur | A. M. McIntosh |
URL | http://www.nature.com/mp/journal/v21/n3/full/mp201512a.html |
Autorisations | © 2015 Nature Publishing Group |
Volume | 21 |
Numéro | 3 |
Pages | 419-425 |
Publication | Molecular Psychiatry |
ISSN | 1359-4184 |
Date | mars 2016 |
Abrév. de revue | Mol Psychiatry |
DOI | 10.1038/mp.2015.12 |
Consulté le | 09/05/2016 à 01:32:43 |
Catalogue de bibl. | www.nature.com |
Langue | en |
Résumé | Cognitive impairment is common among individuals diagnosed with autism spectrum disorder (ASD) and attention-deficit hyperactivity disorder (ADHD). It has been suggested that some aspects of intelligence are preserved or even superior in people with ASD compared with controls, but consistent evidence is lacking. Few studies have examined the genetic overlap between cognitive ability and ASD/ADHD. The aim of this study was to examine the polygenic overlap between ASD/ADHD and cognitive ability in individuals from the general population. Polygenic risk for ADHD and ASD was calculated from genome-wide association studies of ASD and ADHD conducted by the Psychiatric Genetics Consortium. Risk scores were created in three independent cohorts: Generation Scotland Scottish Family Health Study (GS:SFHS) (n=9863), the Lothian Birth Cohorts 1936 and 1921 (n=1522), and the Brisbane Adolescent Twin Sample (BATS) (n=921). We report that polygenic risk for ASD is positively correlated with general cognitive ability (beta=0.07, P=6 × 10−7, r2=0.003), logical memory and verbal intelligence in GS:SFHS. This was replicated in BATS as a positive association with full-scale intelligent quotient (IQ) (beta=0.07, P=0.03, r2=0.005). We did not find consistent evidence that polygenic risk for ADHD was associated with cognitive function; however, a negative correlation with IQ at age 11 years (beta=−0.08, Z=−3.3, P=0.001) was observed in the Lothian Birth Cohorts. These findings are in individuals from the general population, suggesting that the relationship between genetic risk for ASD and intelligence is partly independent of clinical state. These data suggest that common genetic variation relevant for ASD influences general cognitive ability. |
Date d'ajout | 09/05/2016 à 01:32:43 |
Modifié le | 09/05/2016 à 01:32:43 |
Type | Article de revue |
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Auteur | G. Davies |
Auteur | A. Tenesa |
Auteur | A. Payton |
Auteur | J. Yang |
Auteur | S. E. Harris |
Auteur | D. Liewald |
Auteur | X. Ke |
Auteur | S. Le Hellard |
Auteur | A. Christoforou |
Auteur | M. Luciano |
Auteur | K. McGhee |
Auteur | L. Lopez |
Auteur | A. J. Gow |
Auteur | J. Corley |
Auteur | P. Redmond |
Auteur | H. C. Fox |
Auteur | P. Haggarty |
Auteur | L. J. Whalley |
Auteur | G. McNeill |
Auteur | M. E. Goddard |
Auteur | T. Espeseth |
Auteur | A. J. Lundervold |
Auteur | I. Reinvang |
Auteur | A. Pickles |
Auteur | V. M. Steen |
Auteur | W. Ollier |
Auteur | D. J. Porteous |
Auteur | M. Horan |
Auteur | J. M. Starr |
Auteur | N. Pendleton |
Auteur | P. M. Visscher |
Auteur | I. J. Deary |
URL | http://www.nature.com/mp/journal/v16/n10/full/mp201185a.html |
Autorisations | © 2011 Nature Publishing Group |
Volume | 16 |
Numéro | 10 |
Pages | 996-1005 |
Publication | Molecular Psychiatry |
ISSN | 1359-4184 |
Date | octobre 2011 |
Abrév. de revue | Mol Psychiatry |
DOI | 10.1038/mp.2011.85 |
Consulté le | 22/05/2016 à 23:34:59 |
Catalogue de bibl. | www.nature.com |
Langue | en |
Résumé | General intelligence is an important human quantitative trait that accounts for much of the variation in diverse cognitive abilities. Individual differences in intelligence are strongly associated with many important life outcomes, including educational and occupational attainments, income, health and lifespan. Data from twin and family studies are consistent with a high heritability of intelligence, but this inference has been controversial. We conducted a genome-wide analysis of 3511 unrelated adults with data on 549 692 single nucleotide polymorphisms (SNPs) and detailed phenotypes on cognitive traits. We estimate that 40% of the variation in crystallized-type intelligence and 51% of the variation in fluid-type intelligence between individuals is accounted for by linkage disequilibrium between genotyped common SNP markers and unknown causal variants. These estimates provide lower bounds for the narrow-sense heritability of the traits. We partitioned genetic variation on individual chromosomes and found that, on average, longer chromosomes explain more variation. Finally, using just SNP data we predicted ~1% of the variance of crystallized and fluid cognitive phenotypes in an independent sample (P=0.009 and 0.028, respectively). Our results unequivocally confirm that a substantial proportion of individual differences in human intelligence is due to genetic variation, and are consistent with many genes of small effects underlying the additive genetic influences on intelligence. |
Date d'ajout | 22/05/2016 à 23:34:59 |
Modifié le | 22/05/2016 à 23:34:59 |
Type | Article de revue |
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Auteur | Sophie Brasseur |
Auteur | Jacques Gregoire |
URL | http://www.necplus.eu/abstract_S0013754510001060 |
Volume | 2010 |
Numéro | 01 |
Pages | 59 |
Publication | Enfance |
ISSN | 0013-7545, 1969-6981 |
Date | 3/2010 |
DOI | 10.4074/S0013754510001060 |
Consulté le | 11/05/2016 à 22:24:39 |
Catalogue de bibl. | CrossRef |
Langue | en |
Titre abrégé | L’intelligence émotionnelle – trait chez les adolescents à haut potentiel |
Date d'ajout | 11/05/2016 à 22:24:39 |
Modifié le | 11/05/2016 à 22:24:39 |
Type | Article de revue |
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Auteur | Joanne Ruthsatz |
Auteur | Stephen A. Petrill |
Auteur | Ning Li |
Auteur | Samuel L. Wolock |
Auteur | Christopher W. Bartlett |
Volume | 79 |
Numéro | 2 |
Pages | 53-59 |
Publication | Human Heredity |
ISSN | 1423-0062 |
Date | 2015 |
Extra | PMID: 25791271 |
Abrév. de revue | Hum. Hered. |
DOI | 10.1159/000373890 |
Catalogue de bibl. | PubMed |
Langue | eng |
Résumé | Child prodigies are rare individuals with an exceptional working memory and unique attentional skills that may facilitate the attainment of professional skill levels at an age well before what is observed in the general population. Some characteristics of prodigy have been observed to be quantitatively similar to those observed in autism spectrum disorder (ASD), suggesting possible shared etiology, though objectively validated prodigies are so rare that evidence has been sparse. We performed a family-based genome-wide linkage analysis on 5 nuclear and extended families to search for genetic loci that influence the presence of both prodigy and ASD, assuming that the two traits have the same genetic etiology in the analysis model in order to find shared loci. A shared locus on chromosome 1p31-q21 reached genome-wide significance with two extended family-based linkage methods consisting of the Bayesian PPL method and the LOD score maximized over the trait parameters (i.e., MOD), yielding a simulation-based empirical significance of p = 0.000742 and p = 0.000133, respectively. Within linkage regions, we performed association analysis and assessed if copy number variants could account for the linkage signal. No evidence of specificity for either the prodigy or the ASD trait was observed. This finding suggests that a locus on chromosome 1 increases the likelihood of both prodigy and autism in these families. |
Date d'ajout | 22/05/2016 à 23:13:05 |
Modifié le | 22/05/2016 à 23:13:05 |
Type | Article de revue |
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Auteur | Francesca Happé |
Auteur | Uta Frith |
URL | http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2677594/ |
Volume | 364 |
Numéro | 1522 |
Pages | 1345-1350 |
Publication | Philosophical Transactions of the Royal Society B: Biological Sciences |
ISSN | 0962-8436 |
Date | 2009-5-27 |
Extra | PMID: 19528016 PMCID: PMC2677594 |
Abrév. de revue | Philos Trans R Soc Lond B Biol Sci |
DOI | 10.1098/rstb.2009.0009 |
Consulté le | 16/05/2016 à 00:08:40 |
Catalogue de bibl. | PubMed Central |
Date d'ajout | 16/05/2016 à 00:08:40 |
Modifié le | 16/05/2016 à 00:08:40 |