1. Balogh R, Lin E, Dobranowski K, Selick A, Wilton AS, Lunsky Y. {{All-Cause, 30-Day Readmissions Among Persons With Intellectual and Developmental Disabilities and Mental Illness}}. {Psychiatr Serv}. 2017: appips201600534.
OBJECTIVE: Early hospital readmissions within 30 days of discharge are common and costly. This research describes predictors of all-cause, 30-day hospital readmissions among persons with intellectual and developmental disabilities (IDD), a group known to experience high rates of hospitalization. METHODS: A cohort of 66,484 adults with IDD from Ontario, Canada, was used to create two subgroups: individuals with IDD only and those with IDD and mental illness. The rates of hospital readmission were determined and contrasted with a comparison subgroup of people without IDD who have mental illness. RESULTS: Compared with those with mental illness only, individuals with IDD and mental illness were 1.7 times more likely to experience a hospital readmission within 30 days. Predictors of their readmission rates included being a young adult and having high morbidity levels. CONCLUSIONS: The high rate of hospital readmission suggests that individuals with IDD and mental illness need attention regarding discharge planning and outpatient follow-up.
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2. Gouleme N, Scheid I, Peyre H, Seassau M, Maruani A, Clarke J, Delorme R, Bucci MP. {{Postural Control and Emotion in Children with Autism Spectrum Disorders}}. {Transl Neurosci}. 2017; 8: 158-66.
Autism Spectrum Disorders subjects (ASD) are well known to have deficits in social interaction. We recorded simultaneously eye movements and postural sway during exploration of emotional faces in children with ASD and typically developing children (TD). We analyzed several postural and ocular parameters. The results showed that all postural parameters were significantly greater in children with ASD; ASD made significantly fewer saccades and had shorter fixation time than TD, particularly in the eyes, and especially for unpleasant emotions. These results suggest that poor postural control of ASD and their impaired visual strategies could be due to a lack of interest in social cognition, causing a delay in the development of the cortical areas, and thus could have an effect on their postural control.
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3. Hartley C, Trainer A, Allen ML. {{Investigating the relationship between language and picture understanding in children with autism spectrum disorder}}. {Autism}. 2017: 1362361317729613.
Previous studies report that minimally verbal children with autism spectrum disorder show impaired picture comprehension when matched to typically developing controls on language comprehension. Here, we compare both picture comprehension and picture production abilities in linguistically delayed children with autism spectrum disorder and typically developing controls matched on language comprehension and language production. Participants were 20 children with autism spectrum disorder ( M age: 11.2 years) and 20 typically developing children ( M age: 4.4 years) matched on age equivalents for receptive language (autism spectrum disorder, M: 4.6 years; typically developing, M: 4.5 years) and expressive language (autism spectrum disorder, M: 4.4 years; typically developing, M: 4.5 years). Picture comprehension was assessed by asking children to identify the three-dimensional referents of line drawings. Picture production was assessed by asking children to create representational drawings of unfamiliar objects and having raters identify their referents. The results of both picture tasks revealed statistically equivalent performance for typically developing children and children with autism spectrum disorder, and identical patterns of performance across trial types. These findings suggest that early deficits in pictorial understanding displayed by minimally verbal individuals may diminish as their expressive language skills develop. Theoretically, our study indicates that development in linguistic and pictorial domains may be inter-related for children with autism spectrum disorder (as is the case for typical development).
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4. Suarez MA. {{Laboratory Food Acceptance in Children With Autism Spectrum Disorder Compared With Children With Typical Development}}. {Am J Occup Ther}. 2017; 71(6): 7106220020p1-p6.
Studies using parent-report measures have described the high prevalence of food selectivity in children with autism spectrum disorder (ASD). However, few studies have documented food acceptance in a controlled laboratory environment. The objective of this study was to compare laboratory food acceptance in children with ASD with that of children with typical development (TD). In addition, the relationships between food acceptance and the child’s age, sensory processing pattern, and autism severity were explored. Results indicate that children with autism (n = 31) accepted fewer foods in the laboratory environment than the children with TD (n = 21) and that food acceptance was related to age but not to ASD severity. In addition, sensory processing scores were associated with food acceptance for the combined ASD and TD groups. Results are discussed in the context of the literature. This information has the potential to support evaluation and treatment of food selectivity.
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5. Tu S, Akhtar MW, Escorihuela RM, Amador-Arjona A, Swarup V, Parker J, Zaremba JD, Holland T, Bansal N, Holohan DR, Lopez K, Ryan SD, Chan SF, Yan L, Zhang X, Huang X, Sultan A, McKercher SR, Ambasudhan R, Xu H, Wang Y, Geschwind DH, Roberts AJ, Terskikh AV, Rissman RA, Masliah E, Lipton SA, Nakanishi N. {{NitroSynapsin therapy for a mouse MEF2C haploinsufficiency model of human autism}}. {Nat Commun}. 2017; 8(1): 1488.
Transcription factor MEF2C regulates multiple genes linked to autism spectrum disorder (ASD), and human MEF2C haploinsufficiency results in ASD, intellectual disability, and epilepsy. However, molecular mechanisms underlying MEF2C haploinsufficiency syndrome remain poorly understood. Here we report that Mef2c (+/-)(Mef2c-het) mice exhibit behavioral deficits resembling those of human patients. Gene expression analyses on brains from these mice show changes in genes associated with neurogenesis, synapse formation, and neuronal cell death. Accordingly, Mef2c-het mice exhibit decreased neurogenesis, enhanced neuronal apoptosis, and an increased ratio of excitatory to inhibitory (E/I) neurotransmission. Importantly, neurobehavioral deficits, E/I imbalance, and histological damage are all ameliorated by treatment with NitroSynapsin, a new dual-action compound related to the FDA-approved drug memantine, representing an uncompetitive/fast off-rate antagonist of NMDA-type glutamate receptors. These results suggest that MEF2C haploinsufficiency leads to abnormal brain development, E/I imbalance, and neurobehavioral dysfunction, which may be mitigated by pharmacological intervention.
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6. Vogel Ciernia A, Careaga M, LaSalle JM, Ashwood P. {{Microglia from offspring of dams with allergic asthma exhibit epigenomic alterations in genes dysregulated in autism}}. {Glia}. 2017.
Dysregulation in immune responses during pregnancy increases the risk of a having a child with an autism spectrum disorder (ASD). Asthma is one of the most common chronic diseases among pregnant women, and symptoms often worsen during pregnancy. We recently developed a mouse model of maternal allergic asthma (MAA) that induces changes in sociability, repetitive, and perseverative behaviors in the offspring. Since epigenetic changes help a static genome adapt to the maternal environment, activation of the immune system may epigenetically alter fetal microglia, the brain’s resident immune cells. We therefore tested the hypothesis that epigenomic alterations to microglia may be involved in behavioral abnormalities observed in MAA offspring. We used the genome-wide approaches of whole genome bisulfite sequencing to examine DNA methylation and RNA sequencing to examine gene expression in microglia from juvenile MAA offspring. Differentially methylated regions were enriched for immune signaling pathways and important microglial developmental transcription factor binding motifs. Differential expression analysis identified genes involved in controlling microglial sensitivity to the environment and shaping neuronal connections in the developing brain. Differentially expressed genes significantly overlapped genes with altered expression in human ASD cortex, supporting a role for microglia in the pathogenesis of ASD.
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7. Wang W, Cox BM, Jia Y, Le AA, Cox CD, Jung KM, Hou B, Piomelli D, Gall CM, Lynch G. {{Treating a novel plasticity defect rescues episodic memory in Fragile X model mice}}. {Mol Psychiatry}. 2017.
Episodic memory, a fundamental component of human cognition, is significantly impaired in autism. We believe we report the first evidence for this problem in the Fmr1-knockout (KO) mouse model of Fragile X syndrome and describe potentially treatable underlying causes. The hippocampus is critical for the formation and use of episodes, with semantic (cue identity) information relayed to the structure via the lateral perforant path (LPP). The unusual form of synaptic plasticity expressed by the LPP (lppLTP) was profoundly impaired in Fmr1-KOs relative to wild-type mice. Two factors contributed to this defect: (i) reduced GluN1 subunit levels in synaptic NMDA receptors and related currents, and (ii) impaired retrograde synaptic signaling by the endocannabinoid 2-arachidonoylglycerol (2-AG). Studies using a novel serial cue paradigm showed that episodic encoding is dependent on both the LPP and the endocannabinoid receptor CB1, and is strikingly impaired in Fmr1-KOs. Enhancing 2-AG signaling rescued both lppLTP and learning in the mutants. Thus, two consequences of the Fragile-X mutation converge on plasticity at one site in hippocampus to prevent encoding of a basic element of cognitive memory. Collectively, the results suggest a clinically plausible approach to treatment.Molecular Psychiatry advance online publication, 14 November 2017; doi:10.1038/mp.2017.221.
