12 recherche sur le mot-clé 'prefrontal cortex'

Neuron density is decreased in the prefrontal cortex in Williams syndrome / Caroline HORTON LEW in Autism Research, 10-1 (January 2017)  

Public ISBD [article]  inAutism Research > 10-1 (January 2017) . - p.99-112 Titre : Neuron density is decreased in the prefrontal cortex in Williams syndrome Type de document : Texte imprimé et/ou numérique Auteurs : Caroline HORTON LEW, Auteur ; Chelsea BROWN, Auteur ; Ursula BELLUGI, Auteur ; Katerina SEMENDEFERI, Auteur Article en page(s) : p.99-112 Langues : Anglais (eng) Mots-clés : frontal pole  design-based stereology  cytoarchitecture  Williams syndrome  prefrontal cortex  neuron density Index. décimale : PER Périodiques Résumé : Williams Syndrome (WS) is a rare neurodevelopmental disorder associated with a hemideletion in chromosome 7, which manifests a distinct behavioral phenotype characterized by a hyperaffiliative social drive, in striking contrast to the social avoidance behaviors that are common in Autism Spectrum Disorder (ASD). MRI studies have observed structural and functional abnormalities in WS cortex, including the prefrontal cortex (PFC), a region implicated in social cognition. This study utilizes the Bellugi Williams Syndrome Brain Collection, a unique resource that comprises the largest WS postmortem brain collection in existence, and is the first to quantitatively examine WS PFC cytoarchitecture. We measured neuron density in layers II/III and V/VI of five cortical areas: PFC areas BA 10 and BA 11, primary motor BA 4, primary somatosensory BA 3, and visual area BA 18 in six matched pairs of WS and typically developing (TD) controls. Neuron density in PFC was lower in WS relative to TD, with layers V/VI demonstrating the largest decrease in density, reaching statistical significance in BA 10. In contrast, BA 3 and BA 18 demonstrated a higher density in WS compared to TD, although this difference was not statistically significant. Neuron density in BA 4 was similar in WS and TD. While other cortical areas were altered in WS, prefrontal areas appeared to be most affected. Neuron density is also altered in the PFC of individuals with ASD. Together these findings suggest that the PFC is targeted in neurodevelopmental disorders associated with sociobehavioral alterations. En ligne : http://dx.doi.org/10.1002/aur.1677 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=303 [article] Neuron density is decreased in the prefrontal cortex in Williams syndrome [Texte imprimé et/ou numérique] / Caroline HORTON LEW, Auteur ; Chelsea BROWN, Auteur ; Ursula BELLUGI, Auteur ; Katerina SEMENDEFERI, Auteur . - p.99-112. Langues : Anglais (eng) in Autism Research > 10-1 (January 2017) . - p.99-112 Mots-clés : frontal pole  design-based stereology  cytoarchitecture  Williams syndrome  prefrontal cortex  neuron density Index. décimale : PER Périodiques Résumé : Williams Syndrome (WS) is a rare neurodevelopmental disorder associated with a hemideletion in chromosome 7, which manifests a distinct behavioral phenotype characterized by a hyperaffiliative social drive, in striking contrast to the social avoidance behaviors that are common in Autism Spectrum Disorder (ASD). MRI studies have observed structural and functional abnormalities in WS cortex, including the prefrontal cortex (PFC), a region implicated in social cognition. This study utilizes the Bellugi Williams Syndrome Brain Collection, a unique resource that comprises the largest WS postmortem brain collection in existence, and is the first to quantitatively examine WS PFC cytoarchitecture. We measured neuron density in layers II/III and V/VI of five cortical areas: PFC areas BA 10 and BA 11, primary motor BA 4, primary somatosensory BA 3, and visual area BA 18 in six matched pairs of WS and typically developing (TD) controls. Neuron density in PFC was lower in WS relative to TD, with layers V/VI demonstrating the largest decrease in density, reaching statistical significance in BA 10. In contrast, BA 3 and BA 18 demonstrated a higher density in WS compared to TD, although this difference was not statistically significant. Neuron density in BA 4 was similar in WS and TD. While other cortical areas were altered in WS, prefrontal areas appeared to be most affected. Neuron density is also altered in the PFC of individuals with ASD. Together these findings suggest that the PFC is targeted in neurodevelopmental disorders associated with sociobehavioral alterations. En ligne : http://dx.doi.org/10.1002/aur.1677 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=303

Imbalance of laminar-specific excitatory and inhibitory circuits of the orbitofrontal cortex in autism / Xuefeng LIU in Molecular Autism, 11 (2020)  

Public ISBD [article]  inMolecular Autism > 11 (2020) . - 83 p. Titre : Imbalance of laminar-specific excitatory and inhibitory circuits of the orbitofrontal cortex in autism Type de document : Texte imprimé et/ou numérique Auteurs : Xuefeng LIU, Auteur ; Julied BAUTISTA, Auteur ; Edward LIU, Auteur ; Basilis ZIKOPOULOS, Auteur Article en page(s) : 83 p. Langues : Anglais (eng) Mots-clés : Amygdala  Calbindin  Calretinin  Cortical layers  Emotions  Inhibitory neurons  Myelinated axons  Parvalbumin  Prefrontal cortex  Social interactions Index. décimale : PER Périodiques Résumé : BACKGROUND: The human orbitofrontal cortex (OFC) is involved in assessing the emotional significance of events and stimuli, emotion-based learning, allocation of attentional resources, and social cognition. Little is known about the structure, connectivity and excitatory/inhibitory circuit interactions underlying these diverse functions in human OFC, as well as how the circuit is disrupted in individuals with autism spectrum disorder (ASD). METHODS: We used post-mortem brain tissue from neurotypical adults and individuals with ASD. We examined the morphology and distribution of myelinated axons across cortical layers in OFC, at the single axon level, as a proxy of excitatory pathways. In the same regions, we also examined the laminar distribution of all neurons and neurochemically- and functionally-distinct inhibitory neurons that express the calcium-binding proteins parvalbumin (PV), calbindin (CB), and calretinin (CR). RESULTS: We found that the density of myelinated axons increased consistently towards layer 6, while the average axon diameter did not change significantly across layers in both groups. However, both the density and diameter of myelinated axons were significantly lower in the ASD group compared with the Control group. The distribution pattern and density of the three major types of inhibitory neurons was comparable between groups, but there was a significant reduction in the density of excitatory neurons across OFC layers in ASD. LIMITATIONS: This study is limited by the availability of human post-mortem tissue optimally processed for high-resolution microscopy and immunolabeling, especially from individuals with ASD. CONCLUSIONS: The balance between excitation and inhibition in OFC is at the core of its function, assessing and integrating emotional and social cues with internal states and external inputs. Our preliminary results provide evidence for laminar-specific changes in the ratio of excitation/inhibition in OFC of adults with ASD, with an overall weakening and likely disorganization of excitatory signals and a relative strengthening of local inhibition. These changes likely underlie pathology of major OFC communications with limbic or other cortices and the amygdala in individuals with ASD, and may provide the anatomic basis for disrupted transmission of signals for social interactions and emotions in autism. En ligne : http://dx.doi.org/10.1186/s13229-020-00390-x Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=433 [article] Imbalance of laminar-specific excitatory and inhibitory circuits of the orbitofrontal cortex in autism [Texte imprimé et/ou numérique] / Xuefeng LIU, Auteur ; Julied BAUTISTA, Auteur ; Edward LIU, Auteur ; Basilis ZIKOPOULOS, Auteur . - 83 p. Langues : Anglais (eng) in Molecular Autism > 11 (2020) . - 83 p. Mots-clés : Amygdala  Calbindin  Calretinin  Cortical layers  Emotions  Inhibitory neurons  Myelinated axons  Parvalbumin  Prefrontal cortex  Social interactions Index. décimale : PER Périodiques Résumé : BACKGROUND: The human orbitofrontal cortex (OFC) is involved in assessing the emotional significance of events and stimuli, emotion-based learning, allocation of attentional resources, and social cognition. Little is known about the structure, connectivity and excitatory/inhibitory circuit interactions underlying these diverse functions in human OFC, as well as how the circuit is disrupted in individuals with autism spectrum disorder (ASD). METHODS: We used post-mortem brain tissue from neurotypical adults and individuals with ASD. We examined the morphology and distribution of myelinated axons across cortical layers in OFC, at the single axon level, as a proxy of excitatory pathways. In the same regions, we also examined the laminar distribution of all neurons and neurochemically- and functionally-distinct inhibitory neurons that express the calcium-binding proteins parvalbumin (PV), calbindin (CB), and calretinin (CR). RESULTS: We found that the density of myelinated axons increased consistently towards layer 6, while the average axon diameter did not change significantly across layers in both groups. However, both the density and diameter of myelinated axons were significantly lower in the ASD group compared with the Control group. The distribution pattern and density of the three major types of inhibitory neurons was comparable between groups, but there was a significant reduction in the density of excitatory neurons across OFC layers in ASD. LIMITATIONS: This study is limited by the availability of human post-mortem tissue optimally processed for high-resolution microscopy and immunolabeling, especially from individuals with ASD. CONCLUSIONS: The balance between excitation and inhibition in OFC is at the core of its function, assessing and integrating emotional and social cues with internal states and external inputs. Our preliminary results provide evidence for laminar-specific changes in the ratio of excitation/inhibition in OFC of adults with ASD, with an overall weakening and likely disorganization of excitatory signals and a relative strengthening of local inhibition. These changes likely underlie pathology of major OFC communications with limbic or other cortices and the amygdala in individuals with ASD, and may provide the anatomic basis for disrupted transmission of signals for social interactions and emotions in autism. En ligne : http://dx.doi.org/10.1186/s13229-020-00390-x Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=433

Therapeutic Effects of Bilateral Anodal Transcranial Direct Current Stimulation on Prefrontal and Motor Cortical Areas in Children with Autism Spectrum Disorders: A Pilot Study / Hikmat HADOUSH in Autism Research, 13-5 (May 2020)  

Public ISBD [article]  inAutism Research > 13-5 (May 2020) . - p.828-836 Titre : Therapeutic Effects of Bilateral Anodal Transcranial Direct Current Stimulation on Prefrontal and Motor Cortical Areas in Children with Autism Spectrum Disorders: A Pilot Study Type de document : Texte imprimé et/ou numérique Auteurs : Hikmat HADOUSH, Auteur ; Mohammad NAZZAL, Auteur ; Nihad A. ALMASRI, Auteur ; Hanan KHALIL, Auteur ; Maha ALAFEEF, Auteur Article en page(s) : p.828-836 Langues : Anglais (eng) Mots-clés : autism spectrum disorders  autism treatment evaluation checklist  mirror neurons  prefrontal cortex  transcranial direct current stimulation Index. décimale : PER Périodiques Résumé : Dysfunctional frontal cortical areas associated with clinical features are observed in children with autism spectrum disorder (ASD). This study attempted to identify any potential therapeutic effects of bilateral anodal transcranial direct current stimulation (tDCS) applied over the left and right prefrontal and motor areas on the clinical characteristics of children with ASD. Fifty children with confirmed ASD medical diagnoses were divided equally and randomly into a tDCS treatment group and a control group. The tDCS treatment group underwent 10 sessions (20-min durations, five per week) of bilateral anodal tDCS stimulation applied simultaneously over the left and right prefrontal and motor areas, whereas the control group underwent the same procedures but with the use of sham tDCS stimulation. Total scores and sub-scores of autism treatment evaluation checklist (ATEC) (language and communication; sociability; sensory awareness; and behavioral, health, and physical conditions) were measured before and after the tDCS treatment sessions of both groups. There were significant decreases in total ATEC scores (P = 0.014), sociability sub-scores (P = 0.021), and behavioral, health, and physical condition sub-scores (P = 0.011) in the tDCS treatment group. No significant changes were observed in total ATEC scores and sub-scores in the control group. In conclusion, compared to the control group, bilateral anodal tDCS showed potential therapeutic effects on children with ASD in terms of improvements in sociability, behavior, health, and physical conditions with no reported side effects. Autism Res 2020, 13: 828-836. (c) 2020 International Society for Autism Research, Wiley Periodicals, Inc. LAY SUMMARY: Dysfunctional frontal cortical areas are associated with clinical features in children with autism spectrum disorder (ASD). Transcranial direct current stimulation (tDCS) is found to be a safe, noninvasive method to stimulate cortical regions and thus have therapeutic effects on children with ASD. (c) 2020 International Society for Autism Research, Wiley Periodicals, Inc. En ligne : http://dx.doi.org/10.1002/aur.2290 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=422 [article] Therapeutic Effects of Bilateral Anodal Transcranial Direct Current Stimulation on Prefrontal and Motor Cortical Areas in Children with Autism Spectrum Disorders: A Pilot Study [Texte imprimé et/ou numérique] / Hikmat HADOUSH, Auteur ; Mohammad NAZZAL, Auteur ; Nihad A. ALMASRI, Auteur ; Hanan KHALIL, Auteur ; Maha ALAFEEF, Auteur . - p.828-836. Langues : Anglais (eng) in Autism Research > 13-5 (May 2020) . - p.828-836 Mots-clés : autism spectrum disorders  autism treatment evaluation checklist  mirror neurons  prefrontal cortex  transcranial direct current stimulation Index. décimale : PER Périodiques Résumé : Dysfunctional frontal cortical areas associated with clinical features are observed in children with autism spectrum disorder (ASD). This study attempted to identify any potential therapeutic effects of bilateral anodal transcranial direct current stimulation (tDCS) applied over the left and right prefrontal and motor areas on the clinical characteristics of children with ASD. Fifty children with confirmed ASD medical diagnoses were divided equally and randomly into a tDCS treatment group and a control group. The tDCS treatment group underwent 10 sessions (20-min durations, five per week) of bilateral anodal tDCS stimulation applied simultaneously over the left and right prefrontal and motor areas, whereas the control group underwent the same procedures but with the use of sham tDCS stimulation. Total scores and sub-scores of autism treatment evaluation checklist (ATEC) (language and communication; sociability; sensory awareness; and behavioral, health, and physical conditions) were measured before and after the tDCS treatment sessions of both groups. There were significant decreases in total ATEC scores (P = 0.014), sociability sub-scores (P = 0.021), and behavioral, health, and physical condition sub-scores (P = 0.011) in the tDCS treatment group. No significant changes were observed in total ATEC scores and sub-scores in the control group. In conclusion, compared to the control group, bilateral anodal tDCS showed potential therapeutic effects on children with ASD in terms of improvements in sociability, behavior, health, and physical conditions with no reported side effects. Autism Res 2020, 13: 828-836. (c) 2020 International Society for Autism Research, Wiley Periodicals, Inc. LAY SUMMARY: Dysfunctional frontal cortical areas are associated with clinical features in children with autism spectrum disorder (ASD). Transcranial direct current stimulation (tDCS) is found to be a safe, noninvasive method to stimulate cortical regions and thus have therapeutic effects on children with ASD. (c) 2020 International Society for Autism Research, Wiley Periodicals, Inc. En ligne : http://dx.doi.org/10.1002/aur.2290 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=422

Cellular stress and apoptosis contribute to the pathogenesis of autism spectrum disorder / D. DONG in Autism Research, 11-7 (July 2018)  

Public ISBD [article]  inAutism Research > 11-7 (July 2018) . - p.1076-1090 Titre : Cellular stress and apoptosis contribute to the pathogenesis of autism spectrum disorder Type de document : Texte imprimé et/ou numérique Auteurs : D. DONG, Auteur ; H. R. ZIELKE, Auteur ; D. YEH, Auteur ; P. YANG, Auteur Article en page(s) : p.1076-1090 Langues : Anglais (eng) Mots-clés : apoptosis  cerebellum  endoplasmic reticulum stress  hippocampus  human autism  oxidative stress  prefrontal cortex Index. décimale : PER Périodiques Résumé : The molecular pathogenesis of autism spectrum disorder, a neurodevelopmental disorder, is still elusive. In this study, we investigated the possible roles of endoplasmic reticulum (ER) stress, oxidative stress, and apoptosis as molecular mechanisms underlying autism. This study compared the activation of ER stress signals (protein kinase R-like endoplasmic reticulum kinase [PERK], activating transcription factor 6 [ATF6], inositol-requiring enzyme 1 alpha [IRE1alpha]) in different brain regions (prefrontal cortex, hippocampus, cerebellum) in subjects with autism and in age-matched controls. Our data showed that the activation of three signals of ER stress varies in different regions of the autistic brain. IRE1alpha was activated in cerebellum and prefrontal cortex but ATF6 was activated in hippocampus. PERK was not activated in the three regions. Furthermore, the activation of ER stress was confirmed because the expression of C/EBP-homologous protein (CHOP), which is the common downstream indicators of ER stress signals, and most of ER chaperones were upregulated in the three regions. Consistent with the induction of ER stress, apoptosis was found in the three regions by detecting the cleavage of caspase 8 and poly(ADP-ribose) polymerase as well as using the transferase dUTP nick end labeling assay. Moreover, our data showed that oxidative stress was responsible for ER stress and apoptosis because the levels of 4-Hydroxynonenal and nitrotyrosine-modified proteins were significantly increased in the three regions. In conclusion, these data indicate that cellular stress and apoptosis may play important roles in the pathogenesis of autism. Autism Res 2018, 11: 1076-1090. (c) 2018 International Society for Autism Research, Wiley Periodicals, Inc. LAY SUMMARY: Autism results in significant morbidity and mortality in children. The functional and molecular changes in the autistic brains are unclear. The present study utilized autistic brain tissues from the National Institute of Child Health and Human Development's Brain Tissue Bank for the analysis of cellular and molecular changes in autistic brains. Three key brain regions, the hippocampus, the cerebellum, and the frontal cortex, in six cases of autistic brains and six cases of non-autistic brains from 6 to 16 years old deceased children, were analyzed. The current study investigated the possible roles of endoplasmic reticulum (ER) stress, oxidative stress, and apoptosis as molecular mechanisms underlying autism. The activation of three signals of ER stress (protein kinase R-like endoplasmic reticulum kinase, activating transcription factor 6, inositol-requiring enzyme 1 alpha) varies in different regions. The occurrence of ER stress leads to apoptosis in autistic brains. ER stress may result from oxidative stress because of elevated levels of the oxidative stress markers: 4-Hydroxynonenal and nitrotyrosine-modified proteins in autistic brains. These findings suggest that cellular stress and apoptosis may contribute to the autistic phenotype. Pharmaceuticals and/or dietary supplements, which can alleviate ER stress, oxidative stress and apoptosis, may be effective in ameliorating adverse phenotypes associated with autism. En ligne : http://dx.doi.org/10.1002/aur.1966 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=366 [article] Cellular stress and apoptosis contribute to the pathogenesis of autism spectrum disorder [Texte imprimé et/ou numérique] / D. DONG, Auteur ; H. R. ZIELKE, Auteur ; D. YEH, Auteur ; P. YANG, Auteur . - p.1076-1090. Langues : Anglais (eng) in Autism Research > 11-7 (July 2018) . - p.1076-1090 Mots-clés : apoptosis  cerebellum  endoplasmic reticulum stress  hippocampus  human autism  oxidative stress  prefrontal cortex Index. décimale : PER Périodiques Résumé : The molecular pathogenesis of autism spectrum disorder, a neurodevelopmental disorder, is still elusive. In this study, we investigated the possible roles of endoplasmic reticulum (ER) stress, oxidative stress, and apoptosis as molecular mechanisms underlying autism. This study compared the activation of ER stress signals (protein kinase R-like endoplasmic reticulum kinase [PERK], activating transcription factor 6 [ATF6], inositol-requiring enzyme 1 alpha [IRE1alpha]) in different brain regions (prefrontal cortex, hippocampus, cerebellum) in subjects with autism and in age-matched controls. Our data showed that the activation of three signals of ER stress varies in different regions of the autistic brain. IRE1alpha was activated in cerebellum and prefrontal cortex but ATF6 was activated in hippocampus. PERK was not activated in the three regions. Furthermore, the activation of ER stress was confirmed because the expression of C/EBP-homologous protein (CHOP), which is the common downstream indicators of ER stress signals, and most of ER chaperones were upregulated in the three regions. Consistent with the induction of ER stress, apoptosis was found in the three regions by detecting the cleavage of caspase 8 and poly(ADP-ribose) polymerase as well as using the transferase dUTP nick end labeling assay. Moreover, our data showed that oxidative stress was responsible for ER stress and apoptosis because the levels of 4-Hydroxynonenal and nitrotyrosine-modified proteins were significantly increased in the three regions. In conclusion, these data indicate that cellular stress and apoptosis may play important roles in the pathogenesis of autism. Autism Res 2018, 11: 1076-1090. (c) 2018 International Society for Autism Research, Wiley Periodicals, Inc. LAY SUMMARY: Autism results in significant morbidity and mortality in children. The functional and molecular changes in the autistic brains are unclear. The present study utilized autistic brain tissues from the National Institute of Child Health and Human Development's Brain Tissue Bank for the analysis of cellular and molecular changes in autistic brains. Three key brain regions, the hippocampus, the cerebellum, and the frontal cortex, in six cases of autistic brains and six cases of non-autistic brains from 6 to 16 years old deceased children, were analyzed. The current study investigated the possible roles of endoplasmic reticulum (ER) stress, oxidative stress, and apoptosis as molecular mechanisms underlying autism. The activation of three signals of ER stress (protein kinase R-like endoplasmic reticulum kinase, activating transcription factor 6, inositol-requiring enzyme 1 alpha) varies in different regions. The occurrence of ER stress leads to apoptosis in autistic brains. ER stress may result from oxidative stress because of elevated levels of the oxidative stress markers: 4-Hydroxynonenal and nitrotyrosine-modified proteins in autistic brains. These findings suggest that cellular stress and apoptosis may contribute to the autistic phenotype. Pharmaceuticals and/or dietary supplements, which can alleviate ER stress, oxidative stress and apoptosis, may be effective in ameliorating adverse phenotypes associated with autism. En ligne : http://dx.doi.org/10.1002/aur.1966 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=366

Memory in ASD: have we been barking up the wrong tree? / Jill BOUCHER in Autism, 16-6 (November 2012)  

Public ISBD [article]  inAutism > 16-6 (November 2012) . - p.603-611 Titre : Memory in ASD: have we been barking up the wrong tree? Type de document : Texte imprimé et/ou numérique Auteurs : Jill BOUCHER, Auteur ; Andrew MAYES, Auteur Année de publication : 2012 Article en page(s) : p.603-611 Langues : Anglais (eng) Mots-clés : autism spectrum disorder  memory  hippocampus  prefrontal cortex  parietal cortex  default network Index. décimale : PER Périodiques Résumé : In this theoretical note, possible neural causes of episodic memory impairment in individuals with ASD and currently normal intellectual and linguistic function are considered. The neural causes most commonly argued for are hippocampal or prefrontal cortex dysfunction, associated with impaired neural connectivity. It is argued here that a hippocampal dysfunction hypothesis is weakened by differences in cued recall and paired associate learning in individuals with ASD compared with individuals with developmental or acquired hippocampus-related amnesia, and that recent findings on patients with posterior parietal lesions (PPC) offer a better fit with the dissociation between free and cued recall observed in ASD. The PPC forms part of the default system subserving mindreading, among other functions, and an association between PPC dysfunction and memory impairment in ASD is consistent with recent suggestions that neural disconnectivity within the default system underlies behaviours diagnostic of ASD. En ligne : http://dx.doi.org/10.1177/1362361311417738 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=184 [article] Memory in ASD: have we been barking up the wrong tree? [Texte imprimé et/ou numérique] / Jill BOUCHER, Auteur ; Andrew MAYES, Auteur . - 2012 . - p.603-611. Langues : Anglais (eng) in Autism > 16-6 (November 2012) . - p.603-611 Mots-clés : autism spectrum disorder  memory  hippocampus  prefrontal cortex  parietal cortex  default network Index. décimale : PER Périodiques Résumé : In this theoretical note, possible neural causes of episodic memory impairment in individuals with ASD and currently normal intellectual and linguistic function are considered. The neural causes most commonly argued for are hippocampal or prefrontal cortex dysfunction, associated with impaired neural connectivity. It is argued here that a hippocampal dysfunction hypothesis is weakened by differences in cued recall and paired associate learning in individuals with ASD compared with individuals with developmental or acquired hippocampus-related amnesia, and that recent findings on patients with posterior parietal lesions (PPC) offer a better fit with the dissociation between free and cued recall observed in ASD. The PPC forms part of the default system subserving mindreading, among other functions, and an association between PPC dysfunction and memory impairment in ASD is consistent with recent suggestions that neural disconnectivity within the default system underlies behaviours diagnostic of ASD. En ligne : http://dx.doi.org/10.1177/1362361311417738 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=184

Neural Correlates of Set-Shifting in Children With Autism / Benjamin E. YERYS in Autism Research, 8-4 (August 2015)  

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Neurobiological Mechanisms of Anxiety in ASD / John D. HERRINGTON  

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Effects of a social stimulus on gene expression in a mouse model of fragile X syndrome / T. D. ROGERS in Molecular Autism, 8 (2017)  

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Annual Research Review: Transdiagnostic neuroscience of child and adolescent mental disorders – differentiating decision making in attention-deficit/hyperactivity disorder, conduct disorder, depression, and anxiety / Edmund J. S. SONUGA-BARKE in Journal of Child Psychology and Psychiatry, 57-3 (March 2016)  

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Children with autism spectrum disorder show altered functional connectivity and abnormal maturation trajectories in response to inverted faces / F. MAMASHLI in Autism Research, 14-6 (June 2021)  

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