Centre d'Information et de documentation du CRA Rhône-Alpes
CRA
Informations pratiques
-
Adresse
Centre d'information et de documentation
du CRA Rhône-Alpes
Centre Hospitalier le Vinatier
bât 211
95, Bd Pinel
69678 Bron CedexHoraires
Lundi au Vendredi
9h00-12h00 13h30-16h00Contact
Tél: +33(0)4 37 91 54 65
Mail
Fax: +33(0)4 37 91 54 37
-
Résultat de la recherche
2 recherche sur le mot-clé 'Recognition memory'
Affiner la recherche Générer le flux rss de la recherche
Partager le résultat de cette recherche Faire une suggestion
Object-location memory in adults with autism spectrum disorder / Melanie RING in Autism Research, 8-5 (October 2015)
[article]
Titre : Object-location memory in adults with autism spectrum disorder Type de document : Texte imprimé et/ou numérique Auteurs : Melanie RING, Auteur ; Sebastian B. GAIGG, Auteur ; Dermot M. BOWLER, Auteur Article en page(s) : p.609-619 Langues : Anglais (eng) Mots-clés : explicit relational memory implicit relational memory Autism Spectrum Disorder recognition memory source memory task support hypothesis process-dissociation procedure Index. décimale : PER Périodiques Résumé : This study tested implicit and explicit spatial relational memory in Autism Spectrum Disorder (ASD). Participants were asked to study pictures of rooms and pictures of daily objects for which locations were highlighted in the rooms. Participants were later tested for their memory of the object locations either by being asked to place objects back into their original locations or into new locations. Proportions of times when participants choose the previously studied locations for the objects irrespective of the instruction were used to derive indices of explicit and implicit memory [process-dissociation procedure, Jacoby, 1991, 1998]. In addition, participants performed object and location recognition and source memory tasks where they were asked about which locations belonged to the objects and which objects to the locations. The data revealed difficulty for ASD individuals in actively retrieving object locations (explicit memory) but not in subconsciously remembering them (implicit memory). These difficulties cannot be explained by difficulties in memory for objects or locations per se (i.e., the difficulty pertains to object-location relations). Together these observations lend further support to the idea that ASD is characterised by relatively circumscribed difficulties in relational rather than item-specific memory processes and show that these difficulties extend to the domain of spatial information. They also lend further support to the idea that memory difficulties in ASD can be reduced when support is provided at test. Autism Res 2015, 8: 609–619. © 2015 International Society for Autism Research, Wiley Periodicals, Inc. En ligne : http://dx.doi.org/10.1002/aur.1478 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=270
in Autism Research > 8-5 (October 2015) . - p.609-619[article] Object-location memory in adults with autism spectrum disorder [Texte imprimé et/ou numérique] / Melanie RING, Auteur ; Sebastian B. GAIGG, Auteur ; Dermot M. BOWLER, Auteur . - p.609-619.
Langues : Anglais (eng)
in Autism Research > 8-5 (October 2015) . - p.609-619
Mots-clés : explicit relational memory implicit relational memory Autism Spectrum Disorder recognition memory source memory task support hypothesis process-dissociation procedure Index. décimale : PER Périodiques Résumé : This study tested implicit and explicit spatial relational memory in Autism Spectrum Disorder (ASD). Participants were asked to study pictures of rooms and pictures of daily objects for which locations were highlighted in the rooms. Participants were later tested for their memory of the object locations either by being asked to place objects back into their original locations or into new locations. Proportions of times when participants choose the previously studied locations for the objects irrespective of the instruction were used to derive indices of explicit and implicit memory [process-dissociation procedure, Jacoby, 1991, 1998]. In addition, participants performed object and location recognition and source memory tasks where they were asked about which locations belonged to the objects and which objects to the locations. The data revealed difficulty for ASD individuals in actively retrieving object locations (explicit memory) but not in subconsciously remembering them (implicit memory). These difficulties cannot be explained by difficulties in memory for objects or locations per se (i.e., the difficulty pertains to object-location relations). Together these observations lend further support to the idea that ASD is characterised by relatively circumscribed difficulties in relational rather than item-specific memory processes and show that these difficulties extend to the domain of spatial information. They also lend further support to the idea that memory difficulties in ASD can be reduced when support is provided at test. Autism Res 2015, 8: 609–619. © 2015 International Society for Autism Research, Wiley Periodicals, Inc. En ligne : http://dx.doi.org/10.1002/aur.1478 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=270 Targeting the RHOA pathway improves learning and memory in adult Kctd13 and 16p11.2 deletion mouse models / Sandra MARTIN LORENZO in Molecular Autism, 12 (2021)
[article]
Titre : Targeting the RHOA pathway improves learning and memory in adult Kctd13 and 16p11.2 deletion mouse models Type de document : Texte imprimé et/ou numérique Auteurs : Sandra MARTIN LORENZO, Auteur ; Valérie NALESSO, Auteur ; Claire CHEVALIER, Auteur ; Marie-Christine BIRLING, Auteur ; Yann HERAULT, Auteur Langues : Anglais (eng) Mots-clés : Autism spectrum disorders Copy number variation Intellectual disability Kctd13 Mouse model Neurodevelopment Preclinical treatment Recognition memory Index. décimale : PER Périodiques Résumé : BACKGROUND: Gene copy number variants play an important role in the occurrence of neurodevelopmental disorders. Particularly, the deletion of the 16p11.2 locus is associated with autism spectrum disorder, intellectual disability, and several other features. Earlier studies highlighted the implication of Kctd13 genetic imbalance in 16p11.2 deletion through the regulation of the RHOA pathway. METHODS: Here, we generated a new mouse model with a small deletion of two key exons in Kctd13. Then, we targeted the RHOA pathway to rescue the cognitive phenotypes of the Kctd13 and 16p11.2 deletion mouse models in a pure genetic background. We used a chronic administration of fasudil (HA1077), an inhibitor of the Rho-associated protein kinase, for six weeks in mouse models carrying a heterozygous inactivation of Kctd13, or the deletion of the entire 16p11.2 BP4-BP5 homologous region. RESULTS: We found that the small Kctd13 heterozygous deletion induced a cognitive phenotype similar to the whole deletion of the 16p11.2 homologous region, in the Del/+?mice. We then showed that chronic fasudil treatment can restore object recognition memory in adult heterozygous mutant mice for Kctd13 and for 16p11.2 deletion. In addition, learning and memory improvement occurred in parallel to change in the RHOA pathway. LIMITATIONS: The Kcdt13 mutant line does not recapitulate all the phenotypes found in the 16p11.2 Del/+?model. In particular, the locomotor activity was not altered at 12 and 18 weeks of age and the object location memory was not defective in 18-week old mutants. Similarly, the increase in locomotor activity was not modified by the treatment in the 16p11.2 Del/+?mouse model, suggesting that other loci were involved in such defects. Rescue was observed only after four weeks of treatment but no long-term experiment has been carried out so far. Finally, we did not check the social behaviour, which requires working in another hybrid genetic background. CONCLUSION: These findings confirm KCTD13 as one target gene causing cognitive deficits in 16p11.2 deletion patients, and the relevance of the RHOA pathway as a therapeutic path for 16p11.2 deletion. In addition, they reinforce the contribution of other gene(s) involved in cognitive defects found in the 16p11.2 models in older mice. En ligne : http://dx.doi.org/10.1186/s13229-020-00405-7 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=438
in Molecular Autism > 12 (2021)[article] Targeting the RHOA pathway improves learning and memory in adult Kctd13 and 16p11.2 deletion mouse models [Texte imprimé et/ou numérique] / Sandra MARTIN LORENZO, Auteur ; Valérie NALESSO, Auteur ; Claire CHEVALIER, Auteur ; Marie-Christine BIRLING, Auteur ; Yann HERAULT, Auteur.
Langues : Anglais (eng)
in Molecular Autism > 12 (2021)
Mots-clés : Autism spectrum disorders Copy number variation Intellectual disability Kctd13 Mouse model Neurodevelopment Preclinical treatment Recognition memory Index. décimale : PER Périodiques Résumé : BACKGROUND: Gene copy number variants play an important role in the occurrence of neurodevelopmental disorders. Particularly, the deletion of the 16p11.2 locus is associated with autism spectrum disorder, intellectual disability, and several other features. Earlier studies highlighted the implication of Kctd13 genetic imbalance in 16p11.2 deletion through the regulation of the RHOA pathway. METHODS: Here, we generated a new mouse model with a small deletion of two key exons in Kctd13. Then, we targeted the RHOA pathway to rescue the cognitive phenotypes of the Kctd13 and 16p11.2 deletion mouse models in a pure genetic background. We used a chronic administration of fasudil (HA1077), an inhibitor of the Rho-associated protein kinase, for six weeks in mouse models carrying a heterozygous inactivation of Kctd13, or the deletion of the entire 16p11.2 BP4-BP5 homologous region. RESULTS: We found that the small Kctd13 heterozygous deletion induced a cognitive phenotype similar to the whole deletion of the 16p11.2 homologous region, in the Del/+?mice. We then showed that chronic fasudil treatment can restore object recognition memory in adult heterozygous mutant mice for Kctd13 and for 16p11.2 deletion. In addition, learning and memory improvement occurred in parallel to change in the RHOA pathway. LIMITATIONS: The Kcdt13 mutant line does not recapitulate all the phenotypes found in the 16p11.2 Del/+?model. In particular, the locomotor activity was not altered at 12 and 18 weeks of age and the object location memory was not defective in 18-week old mutants. Similarly, the increase in locomotor activity was not modified by the treatment in the 16p11.2 Del/+?mouse model, suggesting that other loci were involved in such defects. Rescue was observed only after four weeks of treatment but no long-term experiment has been carried out so far. Finally, we did not check the social behaviour, which requires working in another hybrid genetic background. CONCLUSION: These findings confirm KCTD13 as one target gene causing cognitive deficits in 16p11.2 deletion patients, and the relevance of the RHOA pathway as a therapeutic path for 16p11.2 deletion. In addition, they reinforce the contribution of other gene(s) involved in cognitive defects found in the 16p11.2 models in older mice. En ligne : http://dx.doi.org/10.1186/s13229-020-00405-7 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=438