1. Blue ME, Boskey AL, Doty SB, Fedarko NS, Hossain MA, Shapiro JR. {{Osteoblast function and bone histomorphometry in a murine model of Rett syndrome}}. {Bone};2015 (Mar 10)
Rett syndrome (RTT) is an X-linked neurodevelopmental disorder due to mutations affecting the neural transcription factor MeCP2. Approximately 50% of affected females have decreased bone mass. We studied osteoblast function using a murine model of RTT. Female heterozygote (HET) and male Mecp2-null mice were compared to wild type (WT) mice. Micro-CT of tibia from 5week-old Mecp2-null mice showed significant alterations in trabecular bone including reductions in bone volume fraction (-29%), number (-19%), thickness (-9%) and connectivity density (-32%), and increases in trabecular separation (+28%) compared to WT. We also found significant reductions in cortical bone thickness (-18%) and in polar moment of inertia (-45%). In contrast, cortical and trabecular bones from 8week-old WT and HET female mice were not significantly different. However, mineral apposition rate, mineralizing surface and bone formation rate/bone surface were each decreased in HET and Mecp2-null mice compared to WT mice. Histomorphometric analysis of femurs showed decreased numbers of osteoblasts but similar numbers of osteoclasts compared to WT, altered osteoblast morphology and decreased tissue synthesis of alkaline phosphatase in Mecp2-null and HET mice. Osteoblasts cultured from Mecp2-null mice, which unlike WT osteoblasts did not express MeCP2, had increased growth rates, but reductions in mRNA expression of type I collagen, Runx2 and Osterix compared to WT osteoblasts. These results indicate that MeCP2 deficiency leads to altered bone growth. Osteoblast dysfunction was more marked in Mecp2-null null male than in HET female mice, suggesting that expression of MeCP2 plays a critical role in bone development.
Lien vers le texte intégral (Open Access ou abonnement)
2. Ghanizadeh A, Berk M. {{Beta-lactam antibiotics as a possible novel therapy for managing epilepsy and autism, a case report and review of literature}}. {Iran J Child Neurol};2015 (Winter);9(1):99-102.
Autism is a disorder of unknown etiology. There are few FDA approved medications for treating autism. Co-occurring autism and epilepsy is common, and glutamate antagonists improve some symptoms of autism. Ceftriaxone, a beta-lactam antibiotic, increases the expression of the glutamate transporter 1 which decreases extracellular glutamate levels. It is hypothesized that modulating astrocyte glutamate transporter expression by ceftriaxone or cefixime might improve some symptoms of autism. This case report of a child with autism and epilepsy suggests a decrease in seizures after taking cefixime.
3. Gray PH, Edwards DM, O’Callaghan MJ, Gibbons K. {{Screening for autism spectrum disorder in very preterm infants during early childhood}}. {Early Hum Dev};2015 (Mar 9);91(4):271-276.
AIM: The aim of the study was to screen very preterm infants for autism spectrum disorder (ASD) with comparisons to a group of term controls. The study also aimed to identify maternal and neonatal risk factors, development and behaviour associated with a positive screen in the preterm group. METHOD: Preterm infants born </=30weeks gestation and term infants were recruited at two years of age. The mothers were posted the questionnaires and completed the Modified Checklist for Autism in Toddlers (M-CHAT), the Child Behaviour Checklist (CBCL) and the Depression, Anxiety and Stress Scales (DASS). Previously collected data from the mothers at 12months – the Edinburgh Postnatal Depression Scales (EPDS) were analysed. The children had neurodevelopmental assessment including the Bayley-III. Infants positive on M-CHAT screen had an M-CHAT follow-up interview by phone and then were assessed by a developmental paediatrician as indicated with a diagnosis of autism being made on clinical judgement. RESULTS: 13 (13.4%) of the 97 preterm infants screened positive on the M-CHAT compared to three (3.9%) of the 77 term infants (p=0.036). On follow-up interview, three of the preterm infants remained positive (one was diagnosed with autism) compared to none of the term infants. The preterm infants who screened positive were born to younger, non-Caucasian mothers and were of lower birth weight and had a higher incidence of being small for gestational age (SGA). The infants had lower composite scores on Bayley-III and had more internalising and externalising behaviours on the CBCL. The mothers had more emotional problems on the DASS and higher scores on the EPDS. On multivariate analysis, SGA, greater internalising behaviours and higher EPDS scores remained statistically significant. CONCLUSIONS: A positive screen on the M-CHAT occurs more commonly in very preterm infants than those born at term. Internalising behaviours and maternal mental health are associated with a positive screen in the preterm cohort.
Lien vers le texte intégral (Open Access ou abonnement)
4. Hansen M, Armour C, Wang L, Elklit A, Bryant RA. {{Assessing possible DSM-5 ASD subtypes in a sample of victims meeting caseness for DSM-5 ASD based on self-report following multiple forms of traumatic exposure}}. {J Anxiety Disord};2015 (Feb 28);31:84-89.
Acute stress disorder (ASD) was introduced into the DSM-IV to recognize early traumatic responses and as a precursor of PTSD. Although the diagnostic criteria for ASD were altered and structured more similarly to the PTSD definition in DSM-5, only the PTSD diagnosis includes a dissociative subtype. Emerging research has indicated that there also appears to be a highly symptomatic subtype for ASD. However, the specific nature of the subtype is currently unclear. The present study investigates the possible presence of ASD subtypes in a mixed sample of victims meeting caseness for DSM-5 ASD based on self-report following four different types of traumatic exposure (N=472). The results of latent profile analysis revealed a 5-class solution. The highly symptomatic class was marked by high endorsement on avoidance and dissociation compared to the other classes. Findings are discussed in regard to its clinical implications including the implications for the pending the ICD-11 and the recently released DSM-5.
Lien vers le texte intégral (Open Access ou abonnement)
5. Kazim SF, Cardenas-Aguayo Mdel C, Arif M, Blanchard J, Fayyaz F, Grundke-Iqbal I, Iqbal K. {{Sera from Children with Autism Induce Autistic Features Which Can Be Rescued with a CNTF Small Peptide Mimetic in Rats}}. {PLoS One};2015;10(3):e0118627.
Autism is a neurodevelopmental disorder characterized clinically by impairments in social interaction and verbal and non-verbal communication skills as well as restricted interests and repetitive behavior. It has been hypothesized that altered brain environment including an imbalance in neurotrophic support during early development contributes to the pathophysiology of autism. Here we report that sera from children with autism which exhibited abnormal levels of various neurotrophic factors induced cell death and oxidative stress in mouse primary cultured cortical neurons. The effects of sera from autistic children were rescued by pre-treatment with a ciliary neurotrophic factor (CNTF) small peptide mimetic, Peptide 6 (P6), which was previously shown to exert its neuroprotective effect by modulating CNTF/JAK/STAT pathway and LIF signaling and by enhancing brain derived neurotrophic factor (BDNF) expression. Similar neurotoxic effects and neuroinflammation were observed in young Wistar rats injected intracerebroventricularly with autism sera within hours after birth. The autism sera injected rats demonstrated developmental delay and deficits in social communication, interaction, and novelty. Both the neurobiological changes and the behavioral autistic phenotype were ameliorated by P6 treatment. These findings implicate the involvement of neurotrophic imbalance during early brain development in the pathophysiology of autism and a proof of principle of P6 as a potential therapeutic strategy for autism.
Lien vers le texte intégral (Open Access ou abonnement)
6. Khan S, Michmizos K, Tommerdahl M, Ganesan S, Kitzbichler MG, Zetino M, Garel KL, Herbert MR, Hamalainen MS, Kenet T. {{Somatosensory cortex functional connectivity abnormalities in autism show opposite trends, depending on direction and spatial scale}}. {Brain};2015 (Mar 12)
Functional connectivity is abnormal in autism, but the nature of these abnormalities remains elusive. Different studies, mostly using functional magnetic resonance imaging, have found increased, decreased, or even mixed pattern functional connectivity abnormalities in autism, but no unifying framework has emerged to date. We measured functional connectivity in individuals with autism and in controls using magnetoencephalography, which allowed us to resolve both the directionality (feedforward versus feedback) and spatial scale (local or long-range) of functional connectivity. Specifically, we measured the cortical response and functional connectivity during a passive 25-Hz vibrotactile stimulation in the somatosensory cortex of 20 typically developing individuals and 15 individuals with autism, all males and right-handed, aged 8-18, and the mu-rhythm during resting state in a subset of these participants (12 per group, same age range). Two major significant group differences emerged in the response to the vibrotactile stimulus. First, the 50-Hz phase locking component of the cortical response, generated locally in the primary (S1) and secondary (S2) somatosensory cortex, was reduced in the autism group (P < 0.003, corrected). Second, feedforward functional connectivity between S1 and S2 was increased in the autism group (P < 0.004, corrected). During resting state, there was no group difference in the mu-alpha rhythm. In contrast, the mu-beta rhythm, which has been associated with feedback connectivity, was significantly reduced in the autism group (P < 0.04, corrected). Furthermore, the strength of the mu-beta was correlated to the relative strength of 50 Hz component of the response to the vibrotactile stimulus (r = 0.78, P < 0.00005), indicating a shared aetiology for these seemingly unrelated abnormalities. These magnetoencephalography-derived measures were correlated with two different behavioural sensory processing scores (P < 0.01 and P < 0.02 for the autism group, P < 0.01 and P < 0.0001 for the typical group), with autism severity (P < 0.03), and with diagnosis (89% accuracy). A biophysically realistic computational model using data driven feedforward and feedback parameters replicated the magnetoencephalography data faithfully. The direct observation of both abnormally increased and abnormally decreased functional connectivity in autism occurring simultaneously in different functional connectivity streams, offers a potential unifying framework for the unexplained discrepancies in current findings. Given that cortical feedback, whether local or long-range, is intrinsically non-linear, while cortical feedforward is generally linear relative to the stimulus, the present results suggest decreased non-linearity alongside an increased veridical component of the cortical response in autism.
Lien vers le texte intégral (Open Access ou abonnement)
7. Krajmalnik-Brown R, Lozupone C, Kang DW, Adams JB. {{Gut bacteria in children with autism spectrum disorders: challenges and promise of studying how a complex community influences a complex disease}}. {Microb Ecol Health Dis};2015;26:26914.
Recent studies suggest a role for the microbiota in autism spectrum disorders (ASD), potentially arising from their role in modulating the immune system and gastrointestinal (GI) function or from gut-brain interactions dependent or independent from the immune system. GI problems such as chronic constipation and/or diarrhea are common in children with ASD, and significantly worsen their behavior and their quality of life. Here we first summarize previously published data supporting that GI dysfunction is common in individuals with ASD and the role of the microbiota in ASD. Second, by comparing with other publically available microbiome datasets, we provide some evidence that the shifted microbiota can be a result of westernization and that this shift could also be framing an altered immune system. Third, we explore the possibility that gut-brain interactions could also be a direct result of microbially produced metabolites.
Lien vers le texte intégral (Open Access ou abonnement)
8. Martinez RA, Stein JL, Krostag AR, Nelson AM, Marken JS, Menon V, May RC, Yao Z, Kaykas A, Geschwind DH, Grimley JS. {{Genome engineering of isogenic human ES cells to model autism disorders}}. {Nucleic Acids Res};2015 (Mar 11)
Isogenic pluripotent stem cells are critical tools for studying human neurological diseases by allowing one to study the effects of a mutation in a fixed genetic background. Of particular interest are the spectrum of autism disorders, some of which are monogenic such as Timothy syndrome (TS); others are multigenic such as the microdeletion and microduplication syndromes of the 16p11.2 chromosomal locus. Here, we report engineered human embryonic stem cell (hESC) lines for modeling these two disorders using locus-specific endonucleases to increase the efficiency of homology-directed repair (HDR). We developed a system to: (1) computationally identify unique transcription activator-like effector nuclease (TALEN) binding sites in the genome using a new software program, TALENSeek, (2) assemble the TALEN genes by combining golden gate cloning with modified constructs from the FLASH protocol, and (3) test the TALEN pairs in an amplification-based HDR assay that is more sensitive than the typical non-homologous end joining assay. We applied these methods to identify, construct, and test TALENs that were used with HDR donors in hESCs to generate an isogenic TS cell line in a scarless manner and to model the 16p11.2 copy number disorder without modifying genomic loci with high sequence similarity.
Lien vers le texte intégral (Open Access ou abonnement)
9. Moore DJ, Reidy J, Heavey L. {{Attentional allocation of autism spectrum disorder individuals: Searching for a Face-in-the-Crowd}}. {Autism};2015 (Mar 13)
A study is reported which tests the proposition that faces capture the attention of those with autism spectrum disorders less than a typical population. A visual search task based on the Face-in-the-Crowd paradigm was used to examine the attentional allocation of autism spectrum disorder adults for faces. Participants were required to search for discrepant target images from within 9-image arrays. Both participants with autism spectrum disorder and control participants demonstrated speeded identification of faces compared to non-face objects. This indicates that when attention is under conscious control, both autism spectrum disorder and typically developing comparison adults show an attentional bias for faces, which contrasts with previous research which found an absence of an attentional bias for faces in autism spectrum disorder. Theoretical implications of this differentiation are discussed.
Lien vers le texte intégral (Open Access ou abonnement)
10. Mostafa GA, El-Khashab HY, Al-Ayadhi LY. {{A possible association between elevated serum levels of brain-specific auto-antibodies and reduced plasma levels of docosahexaenoic acid in autistic children}}. {J Neuroimmunol};2015 (Mar 15);280:16-20.
Polyunsaturated fatty acids (PUFAs) are not only essential for energy production, but they also exhibit a range of immunomodulatory properties that progress through T cell mediated events. Autoimmunity may have a pathogenic role in a subgroup of autistic children. This study is the first to investigate the relationship between serum levels of anti-myelin basic protein (anti-MBP) brain-specific auto-antibodies and reduced plasma levels of PUFAs in autistic children. Plasma levels of PUFAs (including linoleic, alphalinolenic, arachidonic « AA » and docosahexaenoic « DHA » acids) and serum anti-MBP were measured in 80 autistic children, aged between 4 and 12 years, and 80 healthy-matched children. Autistic patients had significantly lower plasma levels of PUFAs than healthy children. On the other hand, omega6/omega3 ratio (AA/DHA) was significantly higher in autistic patients than healthy children. Low plasma DHA, AA, linolenic and linoleic acids were found in 67.5%, 50%, 40% and 35%, respectively of autistic children. On the other hand, 70% of autistic patients had elevated omega6/omega3 ratio. Autistic patients with increased serum levels of anti-MBP auto-antibodies (75%) had significantly lower plasma DHA (P<0.5) and significantly higher omega6/omega3 ratio (P<0.5) than patients who were seronegative for these antibodies. In conclusions, some autistic children have a significant positive association between reduced levels of plasma DHA and increased serum levels of anti-MBP brain-specific auto-antibodies. However, replication studies of larger samples are recommended to validate whether reduced levels of plasma PUFAs are a mere association or have a role in the induction of the production of anti-MBP in some autistic children.
Lien vers le texte intégral (Open Access ou abonnement)
11. Okazaki R, Takahashi T, Ueno K, Takahashi K, Ishitobi M, Kikuchi M, Higashima M, Wada Y. {{Changes in EEG complexity with electroconvulsive therapy in a patient with autism spectrum disorders: a multiscale entropy approach}}. {Front Hum Neurosci};2015;9:106.
Autism spectrum disorders (ASD) are heterogeneous neurodevelopmental disorders that are reportedly characterized by aberrant neural networks. Recently developed multiscale entropy analysis (MSE) can characterize the complexity inherent in electroencephalography (EEG) dynamics over multiple temporal scales in the dynamics of neural networks. We encountered an 18-year-old man with ASD whose refractory catatonic obsessive-compulsive symptoms were improved dramatically after electroconvulsive therapy (ECT). In this clinical case study, we strove to clarify the neurophysiological mechanism of ECT in ASD by assessing EEG complexity using MSE. Along with ECT, the frontocentral region showed decreased EEG complexity at higher temporal scales, whereas the occipital region expressed an increase at lower temporal scales. Furthermore, these changes were associated with clinical improvement associated with the elevation of brain-derived neurotrophic factor, which is a molecular hypothesis of ECT, playing key roles in ASD pathogenesis. Changes in EEG complexity in a region-specific and temporal scale-specific manner that we found might reflect atypical EEG dynamics in ASD. Although MSE is not a direct approach to measuring neural connectivity and the results are from only a single case, they might reflect specific aberrant neural network activity and the therapeutic neurophysiological mechanism of ECT in ASD.
Lien vers le texte intégral (Open Access ou abonnement)
12. Pace M, Bricout VA. {{Low heart rate response of children with autism spectrum disorders in comparison to controls during physical exercise}}. {Physiol Behav};2015 (Mar 15);141:63-68.
BACKGROUND: The objective of the study was to investigate how the heart rate adjusts during different physical tests. Children with autism spectrum disorder (ASD) do indeed have a lower cardiac response to specific tests. METHODS: Twenty children including 10 subjects with ASD diagnosis and 10 control subjects were evaluated using the Eurofit Physical Fitness Test Battery. During the evaluation, the heart rate was monitored continuously. In parallel, their parents were completed the Vineland Adaptive Behavior Scales. RESULTS: Both groups show the same trend of heart rate increase (during exercise and also during the maximum effort). However, children with ASD presented a significant lower heart rate compared to the control population (p<0.001). Based on Eurofit Physical Fitness Test battery, children with ASD showed lower results than controls on plate tapping test (p<0.01), vertical and broad jump tests (p<0.01) and also sit up test (p<0.01). Moreover, Flamingo balance test showed that the ASD group had a higher number of falls (p<0.01). The handgrip test showed that they had a lower force (p<0.01) and they also executed the find motor educational course more slowly with a significantly higher number of falls, mistakes and omissions (p<0.01). CONCLUSIONS: Both groups showed similar trend with the cardiac kinetic reflecting the adjustment to the effort. However, the significant heart rate decrease of the ASD group during physical test could be due to an alteration of the cardiac response. In addition, the scores obtained by children with ASD on physical tests confirmed the lack of motor abilities such as balance and executive functions.
Lien vers le texte intégral (Open Access ou abonnement)
13. Saldarriaga W, Tassone F, Gonzalez-Teshima LY, Forero-Forero JV, Ayala-Zapata S, Hagerman R. {{Fragile x syndrome}}. {Colomb Med (Cali)};2014 (Oct-Dec);45(4):190-198.
Fragile X Syndrome (FXS) is a genetic disease due to a CGG trinucleotide expansion, named full mutation (greater than 200 CGG repeats), in the fragile X mental retardation 1 gene locus Xq27.3; which leads to an hypermethylated region in the gene promoter therefore silencing it and lowering the expression levels of the fragile X mental retardation 1, a protein involved in synaptic plasticity and maturation. Individuals with FXS present with intellectual disability, autism, hyperactivity, long face, large or prominent ears and macroorchidism at puberty and thereafter. Most of the young children with FXS will present with language delay, sensory hyper arousal and anxiety. Girls are less affected than boys, only 25% have intellectual disability. Given the genomic features of the syndrome, there are patients with a number of triplet repeats between 55 and 200, known as premutation carriers. Most carriers have a normal IQ but some have developmental problems. The diagnosis of FXS has evolved from karyotype with special culture medium, to molecular techniques that are more sensitive and specific including PCR and Southern Blot. During the last decade, the advances in the knowledge of FXS, has led to the development of investigations on pharmaceutical management or targeted treatments for FXS. Minocycline and sertraline have shown efficacy in children.
14. Santos MI, Breda A, Almeida AM. {{Brief Report: Preliminary Proposal of a Conceptual Model of a Digital Environment for Developing Mathematical Reasoning in Students with Autism Spectrum Disorders}}. {J Autism Dev Disord};2015 (Mar 15)
There is clear evidence that in typically developing children reasoning and sense-making are essential in all mathematical learning and understanding processes. In children with autism spectrum disorders (ASD), however, these become much more significant, considering their importance to successful independent living. This paper presents a preliminary proposal of a digital environment, specifically targeted to promote the development of mathematical reasoning in students with ASD. Given the diversity of ASD, the prototyping of this environment requires the study of dynamic adaptation processes and the development of activities adjusted to each user’s profile. We present the results obtained during the first phase of this ongoing research, describing a conceptual model of the proposed digital environment. Guidelines for future research are also discussed.
Lien vers le texte intégral (Open Access ou abonnement)
15. Schunke O, Schottle D, Vettorazzi E, Brandt V, Kahl U, Baumer T, Ganos C, David N, Peiker I, Engel AK, Brass M, Munchau A. {{Mirror me: Imitative responses in adults with autism}}. {Autism};2015 (Mar 13)
Dysfunctions of the human mirror neuron system have been postulated to underlie some deficits in autism spectrum disorders including poor imitative performance and impaired social skills. Using three reaction time experiments addressing mirror neuron system functions under simple and complex conditions, we examined 20 adult autism spectrum disorder participants and 20 healthy controls matched for age, gender and education. Participants performed simple finger-lifting movements in response to (1) biological finger and non-biological dot movement stimuli, (2) acoustic stimuli and (3) combined visual-acoustic stimuli with different contextual (compatible/incompatible) and temporal (simultaneous/asynchronous) relation. Mixed model analyses revealed slower reaction times in autism spectrum disorder. Both groups responded faster to biological compared to non-biological stimuli (Experiment 1) implying intact processing advantage for biological stimuli in autism spectrum disorder. In Experiment 3, both groups had similar ‘interference effects’ when stimuli were presented simultaneously. However, autism spectrum disorder participants had abnormally slow responses particularly when incompatible stimuli were presented consecutively. Our results suggest imitative control deficits rather than global imitative system impairments.
Lien vers le texte intégral (Open Access ou abonnement)
16. Shafritz KM, Bregman JD, Ikuta T, Szeszko PR. {{Neural systems mediating decision-making and response inhibition for social and nonsocial stimuli in autism}}. {Prog Neuropsychopharmacol Biol Psychiatry};2015 (Mar 10);60:112-120.
Autism is marked by impairments in social reciprocity and communication, along with restricted, repetitive and stereotyped behaviors. Prior studies have separately investigated social processing and executive function in autism, but little is known about the brain mechanisms of cognitive control for both emotional and nonemotional stimuli. We used functional magnetic resonance imaging to identify differences in neurocircuitry between individuals with high functioning autism (HFA) and neurotypical controls during two versions of a go/no-go task: emotional (fear and happy faces) and nonemotional (English letters). During the letter task, HFA participants showed hypoactivation in the ventral prefrontal cortex. During the emotion task, happy faces elicited activation in the ventral striatum, nucleus accumbens and anterior amygdala in neurotypical, but not HFA, participants. Response inhibition for fear faces compared with happy faces recruited occipitotemporal regions in HFA, but not neurotypical, participants. In a direct contrast of emotional no-go and letter no-go blocks, HFA participants showed hyperactivation in extrastriate cortex and fusiform gyrus. Accuracy for emotional no-go trials was negatively correlated with activation in fusiform gyrus in the HFA group. These results indicate that autism is associated with abnormal processing in socioemotional brain networks, and support the theory that autism is marked by a social motivational deficit.
Lien vers le texte intégral (Open Access ou abonnement)
17. Skagerberg E, Di Ceglie D, Carmichael P. {{Brief Report: Autistic Features in Children and Adolescents with Gender Dysphoria}}. {J Autism Dev Disord};2015 (Mar 15)
This paper looks at the association between gender dysphoria (GD), scores on the Social Responsiveness Scale (SRS), and reported diagnoses of autism spectrum disorder (ASD). Parents of 166 young people presenting with GD (Mean age = 14.26, SD = 2.68) completed the SRS. Information concerning an ASD diagnosis was also extracted from the patient files. 45.8 % fell within the normal range on the SRS and of those 2.8 % had an ASD diagnosis. 27.1 % fell within the mild/moderate range and of those 15.6 % had an ASD diagnosis and 6.7 % an ASD query. 27.1 % fell within the severe range and of those 24.4 % had an ASD diagnosis and 26.7 % an ASD query. No difference was found in autistic features between the natal females and males.
Lien vers le texte intégral (Open Access ou abonnement)
18. Wang H, Pati S, Pozzo-Miller L, Doering LC. {{Targeted pharmacological treatment of autism spectrum disorders: fragile X and Rett syndromes}}. {Front Cell Neurosci};2015;9:55.
Autism spectrum disorders (ASDs) are genetically and clinically heterogeneous and lack effective medications to treat their core symptoms. Studies of syndromic ASDs caused by single gene mutations have provided insights into the pathophysiology of autism. Fragile X and Rett syndromes belong to the syndromic ASDs in which preclinical studies have identified rational targets for drug therapies focused on correcting underlying neural dysfunction. These preclinical discoveries are increasingly translating into exciting human clinical trials. Since there are significant molecular and neurobiological overlaps among ASDs, targeted treatments developed for fragile X and Rett syndromes may be helpful for autism of different etiologies. Here, we review the targeted pharmacological treatment of fragile X and Rett syndromes and discuss related issues in both preclinical studies and clinical trials of potential therapies for the diseases.
Lien vers le texte intégral (Open Access ou abonnement)
19. Weiss JA, Burnham Riosa P. {{Thriving in Youth with Autism Spectrum Disorder and Intellectual Disability}}. {J Autism Dev Disord};2015 (Mar 15)
Most research on mental health in individuals with autism spectrum disorder (ASD) and intellectual disability (ID) has focused on deficits. We examined individual (i.e., sociocommunicative skills, adaptive behavior, functional cognitive skills) and contextual (i.e., home, school, and community participation) correlates of thriving in 330 youth with ID and ASD compared to youth with ID only, 11-22 years of age (M = 16.74, SD = 2.95). Youth with ASD and ID were reported to thrive less than peers with ID only. Group differences in sociocommunicative ability and school participation mediated the relationship between ASD and less thriving. Research is needed to further elucidate a developmental-contextual framework that can inform interventions to promote mental health and wellness in individuals with ASD and ID.
