Pubmed du 18/01/18

jeudi 18 janvier 2018

1. Autism spectrum disorder in primary care. The Nurse practitioner. 2018 ; 43(2) : 28-9.

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2. Achuta VS, Moykkynen T, Peteri UK, Turconi G, Rivera C, Keinanen K, Castren ML. Functional changes of AMPA responses in human induced pluripotent stem cell-derived neural progenitors in fragile X syndrome. Sci Signal. 2018 ; 11(513).

Altered neuronal network formation and function involving dysregulated excitatory and inhibitory circuits are associated with fragile X syndrome (FXS). We examined functional maturation of the excitatory transmission system in FXS by investigating the response of FXS patient-derived neural progenitor cells to the glutamate analog (AMPA). Neural progenitors derived from induced pluripotent stem cell (iPSC) lines generated from boys with FXS had augmented intracellular Ca(2+) responses to AMPA and kainate that were mediated by Ca(2+)-permeable AMPA receptors (CP-AMPARs) lacking the GluA2 subunit. Together with the enhanced differentiation of glutamate-responsive cells, the proportion of CP-AMPAR and N-methyl-d-aspartate (NMDA) receptor-coexpressing cells was increased in human FXS progenitors. Differentiation of cells lacking GluA2 was also increased and paralleled the increased inward rectification in neural progenitors derived from Fmr1-knockout mice (the FXS mouse model). Human FXS progenitors had increased the expression of the precursor and mature forms of miR-181a, a microRNA that represses translation of the transcript encoding GluA2. Blocking GluA2-lacking, CP-AMPARs reduced the neurite length of human iPSC-derived control progenitors and further reduced the shortened length of neurites in human FXS progenitors, supporting the contribution of CP-AMPARs to the regulation of progenitor differentiation. Furthermore, we observed reduced expression of Gria2 (the GluA2-encoding gene) in the frontal lobe of FXS mice, consistent with functional changes of AMPARs in FXS. Increased Ca(2+) influx through CP-AMPARs may increase the vulnerability and affect the differentiation and migration of distinct cell populations, which may interfere with normal circuit formation in FXS.

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3. Bakke KA, Howlin P, Retterstol L, Kanavin OJ, Heiberg A, Naerland T. Effect of epilepsy on autism symptoms in Angelman syndrome. Mol Autism. 2018 ; 9 : 2.

Background : Autism spectrum disorder and epilepsy often co-occur ; however, the extent to which the association between autism symptoms and epilepsy is due to shared aetiology or to the direct effects of seizures is a topic of ongoing debate. Angelman syndrome (AS) is presented as a suitable disease model to explore this association. Methods : Data from medical records and questionnaires were used to examine the association between age of epilepsy onset, autism symptoms, genetic aberration and communication level. Forty-eight participants had genetically verified AS (median age 14.5 years ; range 1-57 years). A measure of autism symptoms (the Social Communication Questionnaire ; SCQ) was completed for 38 individuals aged >/= 4 years. Genetic cause was subgrouped into deletion and other genetic aberrations of the 15q11-q13 area. The number of signs used to communicate (< 20 sign and >/= 20 signs) was used as a measure of nonverbal communication. Results : Mean age of epilepsy onset was 3.0 years (range 3 months-7.8 years). Mean SCQ score for individuals without epilepsy was 13.6 (SD = 6.7) and with epilepsy 17.0 (SD = 5.6 ; p = 0.17) ; 58% used fewer than 20 signs to communicate. There were no age differences between groups according to presence of epilepsy, level of nonverbal communication or type of genetic aberration. SCQ scores were higher in individuals with the deletion than in those with other genetic aberrations (18.7 vs 10.8 p = 0.008) and higher in the group who used < 20 signs to communicate (19.4 vs 14.1 p = 0.007). Age of epilepsy onset was correlated with SCQ (r = - 0.61, p < 0.001). Multiple regression showed that age of seizure onset was significantly related to SCQ score (beta = - 0.90 ; p = 0.006), even when the type of genetic abnormality was controlled (R(2) = 0.53 ; F = 10.7 ; p = 0.001). Conclusions : The study provides support for the notion that seizures themselves contribute more to autism symptoms than expected from the underlying genetic pathology alone. The study demonstrates how a rare genetic syndrome such as Angelman syndrome may be used to study the relation between epilepsy and autism symptomatology.

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4. Budimirovic DB, Protic D. FMR1 gene mutations cause neurodevelopmental-degenerative disorders : Importance of fragile X testing in Serbia. Vojnosanitetski pregled. 2016 ; 73(12) : 1089-93.

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5. Cauda F, Nani A, Costa T, Palermo S, Tatu K, Manuello J, Duca S, Fox PT, Keller R. The morphometric co-atrophy networking of schizophrenia, autistic and obsessive spectrum disorders. Hum Brain Mapp. 2018.

By means of a novel methodology that can statistically derive patterns of co-alterations distribution from voxel-based morphological data, this study analyzes the patterns of brain alterations of three important psychiatric spectra-that is, schizophrenia spectrum disorder (SCZD), autistic spectrum disorder (ASD), and obsessive-compulsive spectrum disorder (OCSD). Our analysis provides five important results. First, in SCZD, ASD, and OCSD brain alterations do not distribute randomly but, rather, follow network-like patterns of co-alteration. Second, the clusters of co-altered areas form a net of alterations that can be defined as morphometric co-alteration network or co-atrophy network (in the case of gray matter decreases). Third, within this network certain cerebral areas can be identified as pathoconnectivity hubs, the alteration of which is supposed to enhance the development of neuronal abnormalities. Fourth, within the morphometric co-atrophy network of SCZD, ASD, and OCSD, a subnetwork composed of eleven highly connected nodes can be distinguished. This subnetwork encompasses the anterior insulae, inferior frontal areas, left superior temporal areas, left parahippocampal regions, left thalamus and right precentral gyri. Fifth, the co-altered areas also exhibit a normal structural covariance pattern which overlaps, for some of these areas (like the insulae), the co-alteration pattern. These findings reveal that, similarly to neurodegenerative diseases, psychiatric disorders are characterized by anatomical alterations that distribute according to connectivity constraints so as to form identifiable morphometric co-atrophy patterns.

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6. Guo M, Zhu J, Yang T, Lai X, Lei Y, Chen J, Li T. Vitamin A and vitamin D deficiencies exacerbate symptoms in children with autism spectrum disorders. Nutr Neurosci. 2018 : 1-11.

OBJECTIVES : This study was designed to investigate the vitamin A (VA) and vitamin D (VD) levels in children with autism spectrum disorders (ASD) and to determine whether co-deficiency of VA and VD exacerbates clinical symptoms in autistic children. METHODS : The Autism Behavior Checklist, Childhood Autism Rating Scale (CARS), and Social Responsiveness Scale (SRS) were used to assess the symptoms of 332 children diagnosed as ASD. And the Gesell Developmental Scale (GDS) was used to evaluate neurodevelopment in children with ASD. Anthropometric measurement and questionnaire results were compared for all autistic children and 197 age- and gender-matched control children. Serum retinol levels were detected with high-performance liquid chromatography, and serum levels of 25-OH vitamin D were measured with an immunoassay method in the two groups. RESULTS : The ZHA, ZWA, and ZBMIA of the children with ASD were significantly lower than those of the control children. Furthermore, higher proportions of children with picky eating, resistance to new foods, and eating problems were observed in the ASD group when compared with the control group. Serum retinol and 25-OH vitamin D levels in autistic children were significantly lower than those in the control children. Additionally, VA and VD co-deficiency impacts more on the symptoms and development in autistic children. CONCLUSIONS : We found that children with autism have more VA and VD deficiencies than control children, and VA and VD co-deficiency may exacerbate the symptoms of children with ASD.

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7. Jin Y, Choi J, Won J, Hong Y. The Relationship between Autism Spectrum Disorder and Melatonin during Fetal Development. Molecules (Basel, Switzerland). 2018 ; 23(1).

The aim of this review is to clarify the interrelationship between melatonin and autism spectrum disorder (ASD) during fetal development. ASD refers to a diverse range of neurodevelopmental disorders characterized by social deficits, impaired communication, and stereotyped or repetitive behaviors. Melatonin, which is secreted by the pineal gland, has well-established neuroprotective and circadian entraining effects. During pregnancy, the hormone crosses the placenta into the fetal circulation and transmits photoperiodic information to the fetus allowing the establishment of normal sleep patterns and circadian rhythms that are essential for normal neurodevelopment. Melatonin synthesis is frequently impaired in patients with ASD. The hormone reduces oxidative stress, which is harmful to the central nervous system. Therefore, the neuroprotective and circadian entraining roles of melatonin may reduce the risk of neurodevelopmental disorders such as ASD.

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8. Koberstein JN, Poplawski SG, Wimmer ME, Porcari G, Kao C, Gomes B, Risso D, Hakonarson H, Zhang NR, Schultz RT, Abel T, Peixoto L. Learning-dependent chromatin remodeling highlights noncoding regulatory regions linked to autism. Sci Signal. 2018 ; 11(513).

Autism spectrum disorder (ASD) is a prevalent neurodevelopmental disorder that is associated with genetic risk factors. Most human disease-associated single-nucleotide polymorphisms (SNPs) are not located in genes but rather are in regulatory regions that control gene expression. The function of regulatory regions is determined through epigenetic mechanisms. Parallels between the cellular basis of development and the formation of long-term memory have long been recognized, particularly the role of epigenetic mechanisms in both processes. We analyzed how learning alters chromatin accessibility in the mouse hippocampus using a new high-throughput sequencing bioinformatics strategy we call DEScan (differential enrichment scan). DEScan, which enabled the analysis of data from epigenomic experiments containing multiple replicates, revealed changes in chromatin accessibility at 2365 regulatory regions-most of which were promoters. Learning-regulated promoters were active during forebrain development in mice and were enriched in epigenetic modifications indicative of bivalent promoters. These promoters were disproportionally intronic, showed a complex relationship with gene expression and alternative splicing during memory consolidation and retrieval, and were enriched in the data set relative to known ASD risk genes. Genotyping in a clinical cohort within one of these promoters (SHANK3 promoter 6) revealed that the SNP rs6010065 was associated with ASD. Our data support the idea that learning recapitulates development at the epigenetic level and demonstrate that behaviorally induced epigenetic changes in mice can highlight regulatory regions relevant to brain disorders in patients.

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9. Le Normand MT, Blanc R, Caldani S, Bonnet-Brilhault F. Disrupted behaviour in grammatical morphology in French speakers with autism spectrum disorders. Clinical linguistics & phonetics. 2018 : 1-15.

Mixed and inconsistent findings have been reported across languages concerning grammatical morphology in speakers with Autism Spectrum Disorders (ASD). Some researchers argue for a selective sparing of grammar whereas others claim to have identified grammatical deficits. The present study aimed to investigate this issue in 26 participants with ASD speaking European French who were matched on age, gender and SES to 26 participants with typical development (TD). The groups were compared regarding their productivity and accuracy of syntactic and agreement categories using the French MOR part-of-speech tagger available from the CHILDES. The groups significantly differed in productivity with respect to nouns, adjectives, determiners, prepositions and gender markers. Error analysis revealed that ASD speakers exhibited a disrupted behaviour in grammatical morphology. They made gender, tense and preposition errors and they omitted determiners and pronouns in nominal and verbal contexts. ASD speakers may have a reduced sensitivity to perceiving and processing the distributional structure of syntactic categories when producing grammatical morphemes and agreement categories. The theoretical and cross-linguistic implications of these findings are discussed.

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10. Lipsker CW, von Heijne M, Bolte S, Wicksell RK. A case report and literature review of autism and attention deficit hyperactivity disorder in paediatric chronic pain. Acta paediatrica (Oslo, Norway : 1992). 2018.

Psychiatric disorders are common in paediatric patients with chronic pain, but the overall prevalence of comorbid neurodevelopmental disorders is unclear. We report on a case of severe chronic pain in a child with undiagnosed comorbid autism spectrum disorder (ASD) and attention deficit hyperactivity disorder (ADHD), where significant improvements in pain and function occurred following methylphenidate medication and parental behavioural training. CONCLUSION : The inclusion of behavioural assessment and screening for neurodevelopmental comorbidity may be essential in addressing complex paediatric chronic pain. This article is protected by copyright. All rights reserved.

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11. Liu MJ, Ma LY, Chou WJ, Chen YM, Liu TL, Hsiao RC, Hu HF, Yen CF. Effects of theory of mind performance training on reducing bullying involvement in children and adolescents with high-functioning autism spectrum disorder. PLoS One. 2018 ; 13(1) : e0191271.

Bullying involvement is prevalent among children and adolescents with autism spectrum disorder (ASD). This study examined the effects of theory of mind performance training (ToMPT) on reducing bullying involvement in children and adolescents with high-functioning ASD. Children and adolescents with high-functioning ASD completed ToMPT (n = 26) and social skills training (SST ; n = 23) programs. Participants in both groups and their mothers rated the pretraining and posttraining bullying involvement of participants on the Chinese version of the School Bullying Experience Questionnaire. The paired t test was used to evaluate changes in bullying victimization and perpetration between the pretraining and posttraining assessments. Furthermore, the linear mixed-effect model was used to examine the difference in the training effect between the ToMPT and SST groups. The paired t test indicated that in the ToMPT group, the severities of both self-reported (p = .039) and mother-reported (p = .003) bullying victimization significantly decreased from the pretraining to posttraining assessments, whereas in the SST group, only self-reported bullying victimization significantly decreased (p = .027). The linear mixed-effect model indicated that compared with the SST program, the ToMPT program significantly reduced the severity of mother-reported bullying victimization (p = .041). The present study supports the effects of ToMPT on reducing mother-reported bullying victimization in children and adolescents with high-functioning ASD.

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12. Pallathra AA, Calkins ME, Parish-Morris J, Maddox BB, Perez LS, Miller J, Gur RC, Mandell DS, Schultz RT, Brodkin ES. Defining behavioral components of social functioning in adults with autism spectrum disorder as targets for treatment. Autism Res. 2018.

There is increasing recognition that adults with autism spectrum disorder (ASD) would benefit from treatment to improve social functioning, a key factor in adults’ overall quality of life. However, the various behavioral components of social functioning (i.e., categories of behaviors underlying social functioning), including social motivation, social anxiety, social cognition, and social skills, have not all been assessed together in any sample of adults with ASD, making it difficult to know the relative levels of impairment in these various categories, the relationships among these categories, or promising targets for treatments. We hypothesized there would be significant correlations among measures within the same category, but fewer correlations of measures between categories, indicating the heterogeneity of impairments in adults with ASD. Twenty-nine adults with ASD without co-occurring intellectual disability completed multiple assessments measuring social motivation, social anxiety, social cognition, and social skills, as well as measures of overall ASD symptom levels and community functioning. Results revealed significant positive correlations among measures within most categories ; positive correlations between measures of social motivation and all other categories, except for social cognition ; as well as positive cross-domain correlations between measures of anxiety and ASD phenotype ; measures of social skills and community functioning ; and measures of social skills and ASD phenotype. Further studies are warranted to determine causal relationships among these behavioral categories, across developmental stages. However, the lack of correlations between many categories suggests the potential importance of multidimensional treatments that target the particular components of social functioning most in need of improvement in individuals. Autism Res 2017. (c) 2017 International Society for Autism Research, Wiley Periodicals, Inc. LAY SUMMARY : The goal of this study was to measure behaviors that contribute to social functioning difficulties in adults with ASD, with the ultimate goal of guiding treatment development. We found that motivation to interact with others was significantly related to social anxiety and social skill. Our results suggest that motivation may be important to target in treatment, and that treatments should be tailored to the areas most in need of improvement in each individual.

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13. Riva V, Cantiani C, Mornati G, Gallo M, Villa L, Mani E, Saviozzi I, Marino C, Molteni M. Distinct ERP profiles for auditory processing in infants at-risk for autism and language impairment. Sci Rep. 2018 ; 8(1) : 715.

Early identification of autism spectrum disorder (ASD) is crucial for the formulation of effective intervention programs. Language deficits may be a hallmark feature of ASD and language delay observed in ASD shows striking similarities to that observed in children with language impairment (LI). Auditory processing deficits are seen in both LI and ASD, however, they have not previously been compared directly using Event-Related Potentials (ERPs) in the two at-risk populations. This study aims to characterize infants at-risk for ASD (HR-ASD) at the electrophysiological level and to compare them with infants at-risk for LI (HR-LI) and controls, to find specific markers with predictive value. At 12-month-old, auditory processing in HR-ASD, HR-LI and controls was characterized via ERP oddball paradigm. All infants were then evaluated at 20 months, to investigate the associations between auditory processing and language/ASD-related outcomes. In both HR-ASD and HR-LI, mismatch response latency was delayed compared to controls, whereas only HR-ASD showed overall larger P3 amplitude compared to controls. Interestingly, these ERP measures correlated with later expressive vocabulary and M-CHAT critical items in the whole sample. These results may support the use of objective measurement of auditory processing to delineate pathophysiological mechanisms in ASD, as compared to LI.

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14. Sehlin H, Hedman Ahlstrom B, Andersson G, Wentz E. Experiences of an internet-based support and coaching model for adolescents and young adults with ADHD and autism spectrum disorder -a qualitative study. BMC Psychiatry. 2018 ; 18(1) : 15.

BACKGROUND : There is a great demand for non-medical treatment and support targeting the needs of adolescents and young adults with autism spectrum disorder (ASD) and attention-deficit/hyperactivity disorder (ADHD). There is also a lack of qualitative studies providing in-depth insight into these individuals’ own experiences within this area. The current study aimed to explore how adolescents and young adults with ADHD, ASD or both experienced taking part in an internet-based support and coaching intervention. METHODS : Sixteen participants with ASD, ADHD or both who had participated in an 8-week internet-based support and coaching model, were interviewed using semi-structured interviews. Data was analyzed using qualitative content analysis. RESULTS : Analysis yielded three themes ; Deciding to participate, Taking part in the coaching process and The significance of format. Various motives for joining were expressed by participants, such as viewing the technology as familiar and appealing and expecting it to be better suited to their situation. There was also a previously unfulfilled need for support among participants. In deciding to take part in the intervention the coaches’ competence and knowledge were considered essential, often in the light of previously negative experiences. Taking part in the coaching process meant feeling reassured by having someone to turn to in view of shared obstacles to seeking and receiving help. The support was used for talking through and receiving advice on matters related to their diagnosis. Findings further revealed appreciation for aspects relating to the format such as communicating through the written word, being in one’s own home and an experience of immediacy. Some disadvantages were voiced including incomplete personal interaction and failing technology. There were also suggestions for greater flexibility. CONCLUSIONS : The in-depth qualitative data obtained from this study suggest that the current model of support and the internet-based format have specific qualities that could play an important role in the support of adolescents and young adults with ADHD and ASD. Although not a replacement for face-to-face interaction, it could be a promising complement or alternative to other support and treatment options. TRIAL REGISTRATION : "Internet-based Support for Young People with ADHD and Autism - a Controlled Study" retrospectively registered in www.clinicaltrials.gov ( ClinicalTrials.gov Identifier : NCT02300597 ) at 2014-11-10.

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15. Sikela JM, Searles Quick VB. Genomic trade-offs : are autism and schizophrenia the steep price of the human brain ?. Human genetics. 2018.

Evolution often deals in genomic trade-offs : changes in the genome that are beneficial overall persist even though they also produce disease in a subset of individuals. Here, we explore the possibility that such trade-offs have occurred as part of the evolution of the human brain. Specifically, we provide support for the possibility that the same key genes that have been major contributors to the rapid evolutionary expansion of the human brain and its exceptional cognitive capacity also, in different combinations, are significant contributors to autism and schizophrenia. Furthermore, the model proposes that one of the primary genes behind this trade-off may not technically be "a gene" or "genes" but rather are the highly duplicated sequences that encode the Olduvai protein domain family (formerly called DUF1220). This is not an entirely new idea. Others have proposed that the same genes involved in schizophrenia were also critical to the rapid expansion of the human brain, a view that has been expressed as "the same ’genes’ that drive us mad have made us human". What is new is that a "gene", or more precisely a protein domain family, has been found that may satisfy these requirements.

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16. Tanaka A, Furubayashi T, Arai M, Inoue D, Kimura S, Kiriyama A, Kusamori K, Katsumi H, Yutani R, Sakane T, Yamamoto A. Delivery of oxytocin to the brain for the treatment of autism spectrum disorder by nasal application. Molecular pharmaceutics. 2018.

Oxytocin (OXT) is a cyclic nonapeptide, two amino acids of which are cysteine, forming an intramolecular disulfide bond. OXT is produced in the hypothalamus and is secreted into the blood stream from the posterior pituitary. As recent studies have suggested that OXT is a neurotransmitter exhibiting central effects important for social deficits, it has drawn much attention as a drug candidate for the treatment of autism. Although human-stage clinical trials of the nasal spray of OXT for the treatment of autism have already begun, few studies have examined the pharmacokinetics and brain distribution of OXT after nasal application. The aim of this study is to evaluate the disposition, nasal absorption, and therapeutic potential of OXT after nasal administration. The pharmacokinetics of OXT after intravenous bolus injection to rats followed a two-compartment model, with a rapid initial half-life of 3 min. The nasal bioavailability of OXT was approximately 2%. The brain concentration of OXT after nasal application was much higher than that after intravenous application, despite much lower concentrations in the plasma. More than 95% of OXT in the brain was directly transported from the nasal cavity. The in vivo stress-relief effect by OXT was observed only after intranasal administration. These results indicate that pharmacological active OXT was effectively delivered to the brain after intranasal administration. In conclusion, the nasal cavity is a promising route for the efficient delivery of OXT to the brain.

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17. Valiente-Palleja A, Torrell H, Muntane G, Cortes MJ, Martinez-Leal R, Abasolo N, Alonso Y, Vilella E, Martorell L. Genetic and clinical evidence of mitochondrial dysfunction in autism spectrum disorder and intellectual disability. Hum Mol Genet. 2018.

Clinical conditions commonly associated with mitochondrial disorders (CAMDs) are often present in autism spectrum disorders (ASD) and intellectual disability (ID). Therefore, the mitochondrial dysfunction hypothesis has been proposed as a transversal mechanism that may function in both disorders. Here, we investigated the presence of conditions associated with mitochondrial disorders and mitochondrial DNA (mtDNA) alterations in 122 subjects who presented ASD with ID (ASD group), 115 subjects who presented ID but not ASD (ID group) and 112 healthy controls (HC group). We assessed in the three study groups the presence of the clinical conditions through a questionnaire and the mtDNA content of two mitochondrial genes, MT-ND1 and MT-ND4, by qPCR. The mtDNA sequences of 98 ASD and 95 ID subjects were obtained by mtDNA-targeted next generation sequencing and analyzed through the MToolBox pipeline to identify mtDNA mutations. Subjects with ASD and ID showed higher frequencies of constipation, edema, seizures, vision alterations, strabismus and sphincter incontinence than HCs subjects. ASD and ID subjects showed significantly lower mtDNA content than HCs in both MT-ND1 and MT-ND4 genes. In addition, we identified 49 putative pathogenic variants with a heteroplasmy level higher than 60% : 8 missense, 29 rRNA and 12 tRNA variants. A total of 28.6% of ASD and 30.5% of ID subjects carried at least one putative pathogenic mtDNA mutation. The high frequency of CAMDs, the low mtDNA content and the presence of putative pathogenic mtDNA mutations observed in both ASD and ID subjects are evidence of mitochondrial dysfunction in ASD and ID.

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18. Waitara MS, Stuever M, Eiferman D, Steinberg S. Concomitant Fecal Impaction and Perforated Appendicitis in an Autistic Patient. The American surgeon. 2017 ; 83(12) : 471-3.

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