26 recherche sur le mot-clé 'Animal models'

Probiotics in autism spectrum disorder: Recent insights from animal models / Navid GOLBAGHI in Autism, 28-11 (November 2024)  

Public ISBD [article]  inAutism > 28-11 (November 2024) . - p.2722 - 2737 Titre : Probiotics in autism spectrum disorder: Recent insights from animal models Type de document : texte imprimé Auteurs : Navid GOLBAGHI, Auteur ; Saeideh NAEIMI, Auteur ; Afra DARVISHI, Auteur ; Niloofar NAJARI, Auteur ; Sofia CUSSOTTO, Auteur Article en page(s) : p.2722 - 2737 Langues : Anglais (eng) Mots-clés : Autism Spectrum Disorder  gut-brain axis  Lactobacillus  probiotics  animal models Index. décimale : PER Périodiques Résumé : Autism spectrum disorder is a neurodevelopmental disorder characterized by a wide range of behavioral alterations, including impaired social interaction and repetitive behaviors. Numerous pharmacological interventions have been developed for autism spectrum disorder, often proving ineffective and accompanied by a multitude of side effects. The gut microbial alterations observed in individuals with autism spectrum disorder, including elevated levels of Bacteroidetes, Firmicutes, and Proteobacteria, as well as reduced levels of Bifidobacterium, provide a basis for further investigation. Recent preclinical studies have shown favorable outcomes with probiotic therapy, including improvements in oxidative stress, anti-inflammatory effects, regulation of neurotransmitters, and restoration of microbial balance. The aim of this review is to explore the potential of probiotics for the management and treatment of autism spectrum disorder, by investigating insights from recent studies in animals. Lay abstract Autism spectrum disorder is a neurodevelopmental disorder characterized by a wide range of behavioral alterations, including impaired social interaction and repetitive behaviors. Numerous pharmacological interventions have been developed for autism spectrum disorder, often proving ineffective and accompanied by a multitude of side effects. The gut microbiota is the reservoir of bacteria inhabiting our gastrointestinal tract. The gut microbial alterations observed in individuals with autism spectrum disorder, including elevated levels of Bacteroidetes, Firmicutes, and Proteobacteria, as well as reduced levels of Bifidobacterium, provide a basis for further investigation into the role of the gut microbiota in autism spectrum disorder. Recent preclinical studies have shown favorable outcomes with probiotic therapy, including improvements in oxidative stress, anti-inflammatory effects, regulation of neurotransmitters, and restoration of microbial balance. The aim of this review is to explore the potential of probiotics for the management and treatment of autism spectrum disorder, by investigating insights from recent studies in animals. En ligne : https://dx.doi.org/10.1177/13623613241246911 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=537 [article] Probiotics in autism spectrum disorder: Recent insights from animal models [texte imprimé] / Navid GOLBAGHI, Auteur ; Saeideh NAEIMI, Auteur ; Afra DARVISHI, Auteur ; Niloofar NAJARI, Auteur ; Sofia CUSSOTTO, Auteur . - p.2722 - 2737. Langues : Anglais (eng) in Autism > 28-11 (November 2024) . - p.2722 - 2737 Mots-clés : Autism Spectrum Disorder  gut-brain axis  Lactobacillus  probiotics  animal models Index. décimale : PER Périodiques Résumé : Autism spectrum disorder is a neurodevelopmental disorder characterized by a wide range of behavioral alterations, including impaired social interaction and repetitive behaviors. Numerous pharmacological interventions have been developed for autism spectrum disorder, often proving ineffective and accompanied by a multitude of side effects. The gut microbial alterations observed in individuals with autism spectrum disorder, including elevated levels of Bacteroidetes, Firmicutes, and Proteobacteria, as well as reduced levels of Bifidobacterium, provide a basis for further investigation. Recent preclinical studies have shown favorable outcomes with probiotic therapy, including improvements in oxidative stress, anti-inflammatory effects, regulation of neurotransmitters, and restoration of microbial balance. The aim of this review is to explore the potential of probiotics for the management and treatment of autism spectrum disorder, by investigating insights from recent studies in animals. Lay abstract Autism spectrum disorder is a neurodevelopmental disorder characterized by a wide range of behavioral alterations, including impaired social interaction and repetitive behaviors. Numerous pharmacological interventions have been developed for autism spectrum disorder, often proving ineffective and accompanied by a multitude of side effects. The gut microbiota is the reservoir of bacteria inhabiting our gastrointestinal tract. The gut microbial alterations observed in individuals with autism spectrum disorder, including elevated levels of Bacteroidetes, Firmicutes, and Proteobacteria, as well as reduced levels of Bifidobacterium, provide a basis for further investigation into the role of the gut microbiota in autism spectrum disorder. Recent preclinical studies have shown favorable outcomes with probiotic therapy, including improvements in oxidative stress, anti-inflammatory effects, regulation of neurotransmitters, and restoration of microbial balance. The aim of this review is to explore the potential of probiotics for the management and treatment of autism spectrum disorder, by investigating insights from recent studies in animals. En ligne : https://dx.doi.org/10.1177/13623613241246911 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=537

A comprehensive bioinformatics analysis of circRNA expression in the brain of distinct mouse models of Autism Spectrum Disorder / Guilherme Cordenonsi DA FONSECA ; Carmem GOTTFRIED in Research in Autism Spectrum Disorders, 109 (November 2023)  

Public ISBD [article]  inResearch in Autism Spectrum Disorders > 109 (November 2023) . - 102261 Titre : A comprehensive bioinformatics analysis of circRNA expression in the brain of distinct mouse models of Autism Spectrum Disorder Type de document : texte imprimé Auteurs : Guilherme Cordenonsi DA FONSECA, Auteur ; Carmem GOTTFRIED, Auteur Article en page(s) : 102261 Langues : Anglais (eng) Mots-clés : Autism spectrum disorder  Animal models  Circular RNA  Bioinformatics  NcRNAs Index. décimale : PER Périodiques Résumé : Background Autism Spectrum Disorder (ASD) is a neurodevelopmental condition estimated to affect 1% of individuals worldwide. Its etiology is still not fully understood, but several molecular alterations in ASD are related to noncoding RNAs (ncRNAs). Recently, gene expression of circular RNAs (circRNAs) has been shown to be altered in the brains of autistic individuals and two animal models of ASD. Here we use bioinformatics methods to analyze the gene expression of circRNAs in the brain of six distinct animal models of ASD and identify possible alterations shared between models and between models and humans. Method: six publicly available RNA-Seq data sets were used. CircRNAs were identified by a combination of algorithms using CirComPara2 software. Differentially expressed circRNAs (DECs) were evaluatedwith the Limma Voom method, and the functional profile was evaluated with clusterProfiler. Databases of risk genes and circRNAs altered in ASD were used for translational comparison. Results: We have identified over 130,000 unique circRNAs. DECs per se are shared by a few animal models. However, functional analysis revealed that the DECs from distinct models share a similar profile of changes, mostly related to synaptic structure and function. Regarding translational alterations, around 2% of DECs in mice are orthologous to DECs in autistic individuals. Conclusions: We provide an overview of the expression of circRNAs in mouse models of ASD. The analyses indicate that synaptic circRNAs may be central to the alterations found. We hope the broad identification of circRNAs can help researchers further explore their selected mouse models. En ligne : https://doi.org/10.1016/j.rasd.2023.102261 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=517 [article] A comprehensive bioinformatics analysis of circRNA expression in the brain of distinct mouse models of Autism Spectrum Disorder [texte imprimé] / Guilherme Cordenonsi DA FONSECA, Auteur ; Carmem GOTTFRIED, Auteur . - 102261. Langues : Anglais (eng) in Research in Autism Spectrum Disorders > 109 (November 2023) . - 102261 Mots-clés : Autism spectrum disorder  Animal models  Circular RNA  Bioinformatics  NcRNAs Index. décimale : PER Périodiques Résumé : Background Autism Spectrum Disorder (ASD) is a neurodevelopmental condition estimated to affect 1% of individuals worldwide. Its etiology is still not fully understood, but several molecular alterations in ASD are related to noncoding RNAs (ncRNAs). Recently, gene expression of circular RNAs (circRNAs) has been shown to be altered in the brains of autistic individuals and two animal models of ASD. Here we use bioinformatics methods to analyze the gene expression of circRNAs in the brain of six distinct animal models of ASD and identify possible alterations shared between models and between models and humans. Method: six publicly available RNA-Seq data sets were used. CircRNAs were identified by a combination of algorithms using CirComPara2 software. Differentially expressed circRNAs (DECs) were evaluatedwith the Limma Voom method, and the functional profile was evaluated with clusterProfiler. Databases of risk genes and circRNAs altered in ASD were used for translational comparison. Results: We have identified over 130,000 unique circRNAs. DECs per se are shared by a few animal models. However, functional analysis revealed that the DECs from distinct models share a similar profile of changes, mostly related to synaptic structure and function. Regarding translational alterations, around 2% of DECs in mice are orthologous to DECs in autistic individuals. Conclusions: We provide an overview of the expression of circRNAs in mouse models of ASD. The analyses indicate that synaptic circRNAs may be central to the alterations found. We hope the broad identification of circRNAs can help researchers further explore their selected mouse models. En ligne : https://doi.org/10.1016/j.rasd.2023.102261 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=517

Controlling litter effects to enhance rigor and reproducibility with rodent models of neurodevelopmental disorders / Jessica A. JIMÉNEZ in Journal of Neurodevelopmental Disorders, 13 (2021)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 13 (2021) Titre : Controlling litter effects to enhance rigor and reproducibility with rodent models of neurodevelopmental disorders Type de document : texte imprimé Auteurs : Jessica A. JIMÉNEZ, Auteur ; Mark J. ZYLKA, Auteur Langues : Anglais (eng) Mots-clés : Animals  Female  Haploinsufficiency  Mice  Neurodevelopmental Disorders/chemically induced/genetics  Phenotype  Pregnancy  Reproducibility of Results  Animal models  Litter effect  Neurodevelopmental disorders  Rigor and reproducibility Index. décimale : PER Périodiques Résumé : Research with rodents is crucial for expanding our understanding of genetic and environmental risk factors for neurodevelopmental disorders (NDD). However, there is growing concern about the number of animal studies that are difficult to replicate, potentially undermining the validity of results. These concerns have prompted funding agencies and academic journals to implement more rigorous standards in an effort to increase reproducibility in research. However, these standards fail to address a major source of variability in rodent research brought on by the "litter effect," the fact that rodents from the same litter are phenotypically more similar to one other than rodents from different litters of the same strain. We show that the litter effect accounts for 30-60% of the variability associated with commonly studied phenotypes, including brain, placenta, and body weight. Moreover, we show how failure to control for litter-to-litter variation can mask a phenotype in Chd8(V986*/+) mice that model haploinsufficiency of CHD8, a high-confidence autism gene. Thus, if not properly controlled, the litter effect has the potential to negatively influence rigor and reproducibility of NDD research. While efforts have been made to educate scientists on the importance of controlling for litter effects in previous publications, our analysis of the recent literature (2015-2020) shows that the vast majority of NDD studies focused on genetic risks, including mutant mouse studies, and environmental risks, such as air pollution and valproic acid exposure, do not correct for litter effects or report information on the number of litters used. We outline best practices to help scientists minimize the impact of litter-to-litter variability and to enhance rigor and reproducibility in future NDD studies using rodent models. En ligne : https://dx.doi.org/10.1186/s11689-020-09353-y Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=573 [article] Controlling litter effects to enhance rigor and reproducibility with rodent models of neurodevelopmental disorders [texte imprimé] / Jessica A. JIMÉNEZ, Auteur ; Mark J. ZYLKA, Auteur. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 13 (2021) Mots-clés : Animals  Female  Haploinsufficiency  Mice  Neurodevelopmental Disorders/chemically induced/genetics  Phenotype  Pregnancy  Reproducibility of Results  Animal models  Litter effect  Neurodevelopmental disorders  Rigor and reproducibility Index. décimale : PER Périodiques Résumé : Research with rodents is crucial for expanding our understanding of genetic and environmental risk factors for neurodevelopmental disorders (NDD). However, there is growing concern about the number of animal studies that are difficult to replicate, potentially undermining the validity of results. These concerns have prompted funding agencies and academic journals to implement more rigorous standards in an effort to increase reproducibility in research. However, these standards fail to address a major source of variability in rodent research brought on by the "litter effect," the fact that rodents from the same litter are phenotypically more similar to one other than rodents from different litters of the same strain. We show that the litter effect accounts for 30-60% of the variability associated with commonly studied phenotypes, including brain, placenta, and body weight. Moreover, we show how failure to control for litter-to-litter variation can mask a phenotype in Chd8(V986*/+) mice that model haploinsufficiency of CHD8, a high-confidence autism gene. Thus, if not properly controlled, the litter effect has the potential to negatively influence rigor and reproducibility of NDD research. While efforts have been made to educate scientists on the importance of controlling for litter effects in previous publications, our analysis of the recent literature (2015-2020) shows that the vast majority of NDD studies focused on genetic risks, including mutant mouse studies, and environmental risks, such as air pollution and valproic acid exposure, do not correct for litter effects or report information on the number of litters used. We outline best practices to help scientists minimize the impact of litter-to-litter variability and to enhance rigor and reproducibility in future NDD studies using rodent models. En ligne : https://dx.doi.org/10.1186/s11689-020-09353-y Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=573

Genetic Effects on Cerebellar Structure Across Mouse Models of Autism Using a Magnetic Resonance Imaging Atlas / Patrick E. STEADMAN in Autism Research, 7-1 (February 2014)  

Public ISBD [article]  inAutism Research > 7-1 (February 2014) . - p.124-137 Titre : Genetic Effects on Cerebellar Structure Across Mouse Models of Autism Using a Magnetic Resonance Imaging Atlas Type de document : texte imprimé Auteurs : Patrick E. STEADMAN, Auteur ; Jacob ELLEGOOD, Auteur ; Kamila U. SZULC, Auteur ; Daniel H. TURNBULL, Auteur ; Alexandra L. JOYNER, Auteur ; R. Mark HENKELMAN, Auteur ; Jason P. LERCH, Auteur Article en page(s) : p.124-137 Langues : Anglais (eng) Mots-clés : animal models  neuroimaging  neuroanatomy  structural MRI  genetics Index. décimale : PER Périodiques Résumé : Magnetic resonance imaging (MRI) of autism populations is confounded by the inherent heterogeneity in the individuals' genetics and environment, two factors difficult to control for. Imaging genetic animal models that recapitulate a mutation associated with autism quantify the impact of genetics on brain morphology and mitigate the confounding factors in human studies. Here, we used MRI to image three genetic mouse models with single mutations implicated in autism: Neuroligin-3 R451C knock-in, Methyl-CpG binding protein-2 (MECP2) 308-truncation and integrin β3 homozygous knockout. This study identified the morphological differences specific to the cerebellum, a structure repeatedly linked to autism in human neuroimaging and postmortem studies. To accomplish a comparative analysis, a segmented cerebellum template was created and used to segment each study image. This template delineated 39 different cerebellar structures. For Neuroligin-3 R451C male mutants, the gray (effect size (ES) = 1.94, FDR q = 0.03) and white (ES = 1.84, q = 0.037) matter of crus II lobule and the gray matter of the paraflocculus (ES = 1.45, q = 0.045) were larger in volume. The MECP2 mutant mice had cerebellar volume changes that increased in scope depending on the genotype: hemizygous males to homozygous females. The integrin β3 mutant mouse had a drastically smaller cerebellum than controls with 28 out of 39 cerebellar structures smaller. These imaging results are discussed in relation to repetitive behaviors, sociability, and learning in the context of autism. This work further illuminates the cerebellum's role in autism. En ligne : http://dx.doi.org/10.1002/aur.1344 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=227 [article] Genetic Effects on Cerebellar Structure Across Mouse Models of Autism Using a Magnetic Resonance Imaging Atlas [texte imprimé] / Patrick E. STEADMAN, Auteur ; Jacob ELLEGOOD, Auteur ; Kamila U. SZULC, Auteur ; Daniel H. TURNBULL, Auteur ; Alexandra L. JOYNER, Auteur ; R. Mark HENKELMAN, Auteur ; Jason P. LERCH, Auteur . - p.124-137. Langues : Anglais (eng) in Autism Research > 7-1 (February 2014) . - p.124-137 Mots-clés : animal models  neuroimaging  neuroanatomy  structural MRI  genetics Index. décimale : PER Périodiques Résumé : Magnetic resonance imaging (MRI) of autism populations is confounded by the inherent heterogeneity in the individuals' genetics and environment, two factors difficult to control for. Imaging genetic animal models that recapitulate a mutation associated with autism quantify the impact of genetics on brain morphology and mitigate the confounding factors in human studies. Here, we used MRI to image three genetic mouse models with single mutations implicated in autism: Neuroligin-3 R451C knock-in, Methyl-CpG binding protein-2 (MECP2) 308-truncation and integrin β3 homozygous knockout. This study identified the morphological differences specific to the cerebellum, a structure repeatedly linked to autism in human neuroimaging and postmortem studies. To accomplish a comparative analysis, a segmented cerebellum template was created and used to segment each study image. This template delineated 39 different cerebellar structures. For Neuroligin-3 R451C male mutants, the gray (effect size (ES) = 1.94, FDR q = 0.03) and white (ES = 1.84, q = 0.037) matter of crus II lobule and the gray matter of the paraflocculus (ES = 1.45, q = 0.045) were larger in volume. The MECP2 mutant mice had cerebellar volume changes that increased in scope depending on the genotype: hemizygous males to homozygous females. The integrin β3 mutant mouse had a drastically smaller cerebellum than controls with 28 out of 39 cerebellar structures smaller. These imaging results are discussed in relation to repetitive behaviors, sociability, and learning in the context of autism. This work further illuminates the cerebellum's role in autism. En ligne : http://dx.doi.org/10.1002/aur.1344 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=227

Adult reversal of cognitive phenotypes in neurodevelopmental disorders / Alcino J. SILVA in Journal of Neurodevelopmental Disorders, 1-2 (June 2009)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 1-2 (June 2009) . - p.150-7 Titre : Adult reversal of cognitive phenotypes in neurodevelopmental disorders Type de document : texte imprimé Auteurs : Alcino J. SILVA, Auteur ; Dan EHNINGER, Auteur Article en page(s) : p.150-7 Langues : Anglais (eng) Mots-clés : Animal models  Autism  Neurodevelopmental disorders  Rescue  Treatment Index. décimale : PER Périodiques Résumé : Recent findings in mice suggest that it is possible to reverse certain neurodevelopmental disorders in adults. Changes in development, previously thought to be irreparable in adults, were believed to underlie the neurological and psychiatric phenotypes of a range of common mental health problems with a clear developmental component. As a consequence, most researchers have focused their efforts on understanding the molecular and cellular processes that alter development with the hope that early intervention could prevent the emergent pathology. Unexpectedly, several different animal model studies published recently, including animal models of autism, suggest that it may be possible to reverse neurodevelopmental disorders in adults: Addressing the underlying molecular and cellular deficits in adults could in several cases dramatically improve the neurocognitive phenotypes in these animal models. The findings reviewed here provide hope to millions of individuals afflicted with a wide range of neurodevelopmental disorders, including autism, since they suggest that it may be possible to treat or even cure them in adults. En ligne : http://dx.doi.org/10.1007/s11689-009-9018-7 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=341 [article] Adult reversal of cognitive phenotypes in neurodevelopmental disorders [texte imprimé] / Alcino J. SILVA, Auteur ; Dan EHNINGER, Auteur . - p.150-7. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 1-2 (June 2009) . - p.150-7 Mots-clés : Animal models  Autism  Neurodevelopmental disorders  Rescue  Treatment Index. décimale : PER Périodiques Résumé : Recent findings in mice suggest that it is possible to reverse certain neurodevelopmental disorders in adults. Changes in development, previously thought to be irreparable in adults, were believed to underlie the neurological and psychiatric phenotypes of a range of common mental health problems with a clear developmental component. As a consequence, most researchers have focused their efforts on understanding the molecular and cellular processes that alter development with the hope that early intervention could prevent the emergent pathology. Unexpectedly, several different animal model studies published recently, including animal models of autism, suggest that it may be possible to reverse neurodevelopmental disorders in adults: Addressing the underlying molecular and cellular deficits in adults could in several cases dramatically improve the neurocognitive phenotypes in these animal models. The findings reviewed here provide hope to millions of individuals afflicted with a wide range of neurodevelopmental disorders, including autism, since they suggest that it may be possible to treat or even cure them in adults. En ligne : http://dx.doi.org/10.1007/s11689-009-9018-7 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=341

Altered attentional processing in male and female rats in a prenatal valproic acid exposure model of autism spectrum disorder / Kumari ANSHU in Autism Research, 10-12 (December 2017)  

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Autism-Related Neuroligin-3 Mutation Alters Social Behavior and Spatial Learning / Thomas C. JARAMILLO in Autism Research, 7-2 (April 2014)  

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Better statistical reporting does not lead to statistical rigour: lessons from two decades of pseudoreplication in mouse-model studies of neurological disorders / Constantinos ELEFTHERIOU in Molecular Autism, 16 (2025)  

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Beyond the three-chamber test: toward a multimodal and objective assessment of social behavior in rodents / Renad JABARIN in Molecular Autism, 13 (2022)  

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Brain abnormalities in a Neuroligin3 R451C knockin mouse model associated with autism / Jacob ELLEGOOD in Autism Research, 4-5 (October 2011)  

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