1. Brauna AP, Abreu MH, Resende VL, Castilho LS. {{Risk factors for dental caries in children with developmental disabilities}}. {Braz Oral Res};2016 (Jun 14);30(1)
The aim of the present study was to investigate risk factors for dental caries in children with developmental disabilities who were treated at a clinical reference service for patients with special needs in Belo Horizonte, MG, Brazil. This is a retrospective cohort study that evaluated 401 dental charts of individuals without dental caries or restorations in their first dental appointment. The dependent variable was the time of occurrence of new dental caries or restorations and was measured in months. Gender, age, International Code of Diseases (ICD), mother s education, sugar consumption, use of fluoride toothpaste, oral hygiene, mouth breathing, reports of xerostomia, gingival status, use of psychotropic or asthma drugs, and history of asthma were covariates. The Cox proportional hazards regression model was used to estimate the raw and adjusted hazard ratios and their respective 95% confidence intervals. The average time that individuals remained free of dental caries/restoration was equal to 107.46 months (95%CI 95.41 to 119.51), with a median of caries-free children up to 94 months. For each point increase in the scale of sucrose consumption, the increase in caries risk was 1.07 (95%CI 1.01 to 1.15). Sucrose consumption was the only risk factor for dental caries found in this group of individuals with developmental disabilities.
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2. Cui T, Wang PP, Liu S, Zhang X. {{P300 amplitude and latency in autism spectrum disorder: a meta-analysis}}. {Eur Child Adolesc Psychiatry};2016 (Jun 14)
Autism spectrum disorder (ASD) is an early onset neurodevelopmental disorder. Evidence suggests that ASD patients have abnormalities in information processing. Event-related potential (ERP) technique can directly record brain neural activity in real time. P300 is a positive ERP component which can measure the neuroelectrophysiological characteristics of human beings and has the potential to discover the pathological mechanism of ASD. However, P300 studies on ASD patients are incongruent and the disparities may be caused by several factors. By searching PubMed, Embase and Cochrane Library databases, a meta-analysis of P300 component difference between ASD group and typically developed (TD) control group was conducted. Results of amplitude and latency of P3b and P3a from included studies were synthesized. Random effect model was chosen and standardized mean difference (SMD) was calculated. Subgroup analysis was used to identify the source of heterogeneity and to test the effect of different experiment factors. A total of 407 ASD patients and 457 TD controls from 32 studies were included in this analysis. Reduced amplitude of P3b was found in ASD group (SMD = -0.505, 95 % CI -0.873, -0.138) compared with TD group, but no difference of P3b latency, P3a amplitude, or P3a latency was found between groups. Subgroup analysis showed that oddball paradigm elicited attenuated P3b amplitude in Pz electrode among ASD subjects. This meta-analysis suggests ASD patients have abnormalities in P300 component, which may represent for deficits in cognition, attention orientation and working memory processing, particularly in the decision-making processing condition.
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3. De Felice A, Greco A, Calamandrei G, Minghetti L. {{Prenatal exposure to the organophosphate insecticide chlorpyrifos enhances brain oxidative stress and prostaglandin E2 synthesis in a mouse model of idiopathic autism}}. {J Neuroinflammation};2016;13(1):149.
BACKGROUND: Autism spectrum disorders (ASD) are emerging as polygenic and multifactorial disorders in which complex interactions between defective genes and early exposure to environmental stressors impact on the correct neurodevelopment and brain processes. Organophosphate insecticides, among which chlorpyrifos (CPF), are widely diffused environmental toxicants associated with neurobehavioral deficits and increased risk of ASD occurrence in children. Oxidative stress and dysregulated immune responses are implicated in both organophosphate neurodevelopmental effects and ASD etiopathogenesis. BTBR T+tf/J mice, a well-studied model of idiopathic autism, show several behavioral and immunological alterations found in ASD children, and we recently showed that CPF gestational exposure strengthened some of these autistic-like traits. In the present study, we aimed at investigating whether the behavioral effects of gestational CPF administration are associated with brain increased oxidative stress and altered lipid mediator profile. METHODS: Brain levels of F2-isoprostanes (15-F2t-IsoP), as index of in vivo oxidative stress, and prostaglandin E2 (PGE2), a major arachidonic acid metabolite released by immune cells and by specific glutamatergic neuron populations mainly in cortex and hippocampus, were assessed by specific enzyme-immuno assays in brain homogenates from BTBR T+tf/J and C57Bl6/J mice, exposed during gestation to either vehicle or CPF. Measures were performed in mice of both sexes, at different postnatal stages (PNDs 1, 21, and 70). RESULTS: At birth, BTBR T+tf/J mice exhibited higher baseline 15-F2t-IsoP levels as compared to C57Bl6/J mice, suggestive of greater oxidative stress processes. Gestational treatment with CPF-enhanced 15-F2t-IsoP and PGE2 levels in strain- and age-dependent manner, with 15-F2t-IsoP increased in BTBR T+tf/J mice at PNDs 1 and 21, and PGE2 elevated in BTBR T+tf/J mice at PNDs 21 and 70. At PND 21, CPF effects were sex-dependent being the increase of the two metabolites mainly associated with male mice. CPF treatment also induced a reduction of somatic growth, which reached statistical significance at PND 21. CONCLUSIONS: These findings indicate that the autistic-like BTBR T+tf/J strain is highly vulnerable to environmental stressors during gestational period. The results further support the hypothesis that oxidative stress might be the link between environmental neurotoxicants such as CPF and ASD. The increased levels of oxidative stress during early postnatal life could result in delayed and long-lasting alterations in specific pathways relevant to ASD, of which PGE2 signaling represents an important one.
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4. Dickerson AS, Rahbar MH, Bakian AV, Bilder DA, Harrington RA, Pettygrove S, Kirby RS, Durkin MS, Han I, Moye LA, 3rd, Pearson DA, Wingate MS, Zahorodny WM. {{Autism spectrum disorder prevalence and associations with air concentrations of lead, mercury, and arsenic}}. {Environ Monit Assess};2016 (Jul);188(7):407.
Lead, mercury, and arsenic are neurotoxicants with known effects on neurodevelopment. Autism spectrum disorder (ASD) is a neurodevelopmental disorder apparent by early childhood. Using data on 4486 children with ASD residing in 2489 census tracts in five sites of the Centers for Disease Control and Prevention’s Autism and Developmental Disabilities Monitoring (ADDM) Network, we used multi-level negative binomial models to investigate if ambient lead, mercury, and arsenic concentrations, as measured by the US Environmental Protection Agency National-Scale Air Toxics Assessment (EPA-NATA), were associated with ASD prevalence. In unadjusted analyses, ambient metal concentrations were negatively associated with ASD prevalence. After adjusting for confounding factors, tracts with air concentrations of lead in the highest quartile had significantly higher ASD prevalence than tracts with lead concentrations in the lowest quartile (prevalence ratio (PR) = 1.36; 95 ‘% CI: 1.18, 1.57). In addition, tracts with mercury concentrations above the 75th percentile (>1.7 ng/m(3)) and arsenic concentrations below the 75th percentile (Lien vers le texte intégral (Open Access ou abonnement)
5. Kawanai T, Ago Y, Watanabe R, Inoue A, Taruta A, Onaka Y, Hasebe S, Hashimoto H, Matsuda T, Takuma K. {{Prenatal Exposure to Histone Deacetylase Inhibitors Affects Gene Expression of Autism-Related Molecules and Delays Neuronal Maturation}}. {Neurochem Res};2016 (Jun 14)
Valproic acid (VPA) is a multi-target drug and an inhibitor of histone deacetylase (HDAC). We have previously demonstrated that prenatal exposure to VPA at embryonic day 12.5 (E12.5), but not at E14.5, causes autism-like behavioral abnormalities in male mouse offspring. We have also found that prenatal VPA exposure causes transient histone hyperacetylation in the embryonic brain, followed by decreased neuronal cell numbers in the prefrontal and somatosensory cortices after birth. In the present study, we examined whether prenatal HDAC inhibition affects neuronal maturation in primary mouse cortical neurons. Pregnant mice were injected intraperitoneally with VPA (500 mg/kg) and the more selective HDAC inhibitor trichostatin A (TSA; 500 microg/kg) at E12.5 or E14.5, and primary neuronal cultures were prepared from the cerebral cortices of their embryos. Prenatal exposure to VPA at E12.5, but not at E14.5, decreased total number, total length, and complexity of neuronal dendrites at 14 days in vitro (DIV). The effects of VPA weakened at 21 DIV. Exposure to TSA at E12.5, but not at E14.5, also delayed maturation of cortical neurons. In addition, real-time quantitative PCR revealed that the prenatal exposure to TSA decreased neuroligin-1 (Nlgn1), Shank2, and Shank3 mRNA levels and increased contactin-associated protein-like 2 mRNA level. The delay in neuronal maturation was also observed in Nlgn1-knockdown cells, which were transfected with Nlgn1 siRNA. These findings suggest that prenatal HDAC inhibition causes changes in gene expression of autism-related molecules linked to a delay of neuronal maturation.
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6. Lazaro CP, Ponde MP, Rodrigues LE. {{Opioid peptides and gastrointestinal symptoms in autism spectrum disorders}}. {Rev Bras Psiquiatr};2016 (Jun 14):0.
Autism spectrum disorders (ASDs) are characterized by deficits in the individual’s ability to socialize, communicate, and use the imagination, in addition to stereotyped behaviors. These disorders have a heterogenous phenotype, both in relation to symptoms and regarding severity. Organic problems related to the gastrointestinal tract are often associated with ASD, including dysbiosis, inflammatory bowel disease, exocrine pancreatic insufficiency, celiac disease, indigestion, malabsorption, food intolerance, and food allergies, leading to vitamin deficiencies and malnutrition. In an attempt to explain the pathophysiology involved in autism, a theory founded on opioid excess has been the focus of various investigations, since it partially explains the symptomatology of the disorder. Another hypothesis has been put forward whereby the probable triggers of ASDs would be related to the presence of bacteria in the bowel, oxidative stress, and intestinal permeability. The present update reviews these hypotheses.
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7. Lindstrom R, Lepisto-Paisley T, Vanhala R, Alen R, Kujala T. {{Impaired neural discrimination of emotional speech prosody in children with autism spectrum disorder and language impairment}}. {Neurosci Lett};2016 (Jun 9)
Autism spectrum disorders (ASD) are characterized by deficient social and communication skills, including difficulties in perceiving speech prosody. The present study addressed processing of emotional prosodic changes (sad, scornful and commanding) in natural word stimuli in typically developed school-aged children and in children with ASD and language impairment. We found that the responses to a repetitive word were diminished in amplitude in the children with ASD, reflecting impaired speech encoding. Furthermore, the amplitude of the MMN/LDN component, reflecting cortical discrimination of sound changes, was diminished in the children with ASD for the scornful deviant. In addition, the amplitude of the P3a, reflecting involuntary orienting to attention-catching changes, was diminished in the children with ASD for the scornful deviant and tended to be smaller for the sad deviant. These results suggest that prosody processing in ASD is impaired at various levels of neural processing, including deficient pre-attentive discrimination and involuntary orientation to speech prosody.
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8. Nikvarz N, Alaghband-Rad J, Tehrani-Doost M, Alimadadi A, Ghaeli P. {{Comparing Efficacy and Side Effects of Memantine vs. Risperidone in the Treatment of Autistic Disorder}}. {Pharmacopsychiatry};2016 (Jun 14)
Introduction: This study was aimed to compare the efficacy and side effects of memantine, an antagonist of the NMDA receptor of glutamate, with risperidone given the fact that glutamate has been noted for its possible effects in the pathogenesis of autism. Risperidone, an atypical antipsychotic, has been approved by FDA for the management of irritability associated with autism. Methods: 30 children, aged 4-17 years, entered an 8-week, randomized trial. Patients were randomly assigned to receive either risperidone or memantine. Autism Behavior Checklist (ABC), Childhood Autism Rating Scale (CARS), Clinical Global Impressions – Improvement (CGI-I) and Clinical Global Impression-Severity (CGI-S) scales were used to assess behavioral symptoms of the patients. Results: Both risperidone and memantine reduced the scores of 4 subscales of ABC as well as the 10-item and the total score of CARS significantly. However, differences between the 2 drugs in the scores of each evaluating scale were not found to be significant. Relatively, larger number of patients on risperidone showed « very much improvement » when assessed by CGI-I scale when compared with those on memantine. Discussion and conclusion: The present study suggests that memantine may have beneficial effects in the treatment of many core symptoms of autism. Therefore, memantine may be considered as a potential medication in the treatment of those autistic children who do not respond or cannot tolerate side effects of risperidone.
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9. Orefice LL, Zimmerman AL, Chirila AM, Sleboda SJ, Head JP, Ginty DD. {{Peripheral Mechanosensory Neuron Dysfunction Underlies Tactile and Behavioral Deficits in Mouse Models of ASDs}}. {Cell};2016 (Jun 8)
Patients with autism spectrum disorders (ASDs) commonly experience aberrant tactile sensitivity, yet the neural alterations underlying somatosensory dysfunction and the extent to which tactile deficits contribute to ASD characteristics are unknown. We report that mice harboring mutations in Mecp2, Gabrb3, Shank3, and Fmr1 genes associated with ASDs in humans exhibit altered tactile discrimination and hypersensitivity to gentle touch. Deletion of Mecp2 or Gabrb3 in peripheral somatosensory neurons causes mechanosensory dysfunction through loss of GABAA receptor-mediated presynaptic inhibition of inputs to the CNS. Remarkably, tactile defects resulting from Mecp2 or Gabrb3 deletion in somatosensory neurons during development, but not in adulthood, cause social interaction deficits and anxiety-like behavior. Restoring Mecp2 expression exclusively in the somatosensory neurons of Mecp2-null mice rescues tactile sensitivity, anxiety-like behavior, and social interaction deficits, but not lethality, memory, or motor deficits. Thus, mechanosensory processing defects contribute to anxiety-like behavior and social interaction deficits in ASD mouse models.
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10. Shoffner J, Trommer B, Thurm A, Farmer C, Langley WA, 3rd, Soskey L, Rodriguez AN, D’Souza P, Spence SJ, Hyland K, Swedo SE. {{CSF concentrations of 5-methyltetrahydrofolate in a cohort of young children with autism}}. {Neurology};2016 (Jun 14);86(24):2258-2263.
OBJECTIVE: To examine the association between cerebral folate deficiency and autism, this study examined CSF 5-methyltetrahydrofolate (5-MTHF) concentrations in a group of young children with autism, investigated the natural variation in CSF 5-MTHF over time, and assessed the relationship between CSF 5-MTHF and symptoms. METHODS: CSF was collected from 67 children with a diagnosis of DSM-IV-TR autistic disorder (age, mean +/- SD 43 +/- 11 months), with a second CSF sample obtained 1-3 years later on 31 of these subjects (time to follow-up, 30 +/- 8 months). RESULTS: At time 1, 7% (5/67) of participants had 5-MTHF <40 nmol/L. At follow-up, 23% (7/31) of participants had 5-MTHF <40 nmol/L (only one of whom had been low at time 1). A moderate correlation with a very wide confidence interval (CI) was observed between time 1 and time 2 CSF 5-MTHF measurements (Pearson r[p] = 0.38 [0.04]; 95% CI 0.02-0.64). Neither the CSF 5-MTHF levels nor changes over time correlated with the clinical features of autism. CONCLUSIONS: CSF 5-MTHF levels vary significantly over time in an unpredictable fashion and do not show a significant relationship to typical clinical features of autism. Reduced CSF 5-MTHF levels are a nonspecific finding in autism. Our data do not support the use of lumbar puncture for assessment of CSF 5-MTHF in autism. Lien vers le texte intégral (Open Access ou abonnement)
11. Uljarevic M, Evans DW, Alvares GA, Whitehouse AJ. {{Short report: relationship between restricted and repetitive behaviours in children with autism spectrum disorder and their parents}}. {Mol Autism};2016;7:29.
BACKGROUND: Restricted and repetitive behaviours (RRBs) constitute a core symptom domain of autism spectrum disorder (ASD). However, the nature of RRBs in the context of the Broader Autism Phenotype (BAP) is not well understood. In particular, the relationship between RRBs in ASD probands and their parents remains largely unexplored. The current study explored the link between parental RRBs, measured via Interest in Patterns and Resistance to Changes subscales of the Autism Quotient and their children’s RRBs, measured via Autism Diagnostic Observation Schedule RRB standardized domain score. FINDINGS: Having both parents within the top 20 % of their RRB scores was associated with an increase of RRB scores for their children; however, no parent-of-origin effects were identified. Although the trend was observed for both Interest in Patterns and Resistance to Changes subscale, it was only statistically significant for Interest in Patterns. CONCLUSIONS: This paper provides significant contribution to our understanding of association between RRBs in parents and their children with ASD. Future work should also address the BAP in distinct genetic subtypes (whole chromosome aneuploidies, single gene mutations, copy number variations) of neurodevelopmental and neuropsychiatric disorders that involve RRBs.
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12. Valenti M, Di Giovanni C, Mariano M, Pino MC, Sconci V, Mazza M. {{[Autism after an earthquake: the experience of L’Aquila (Central Italy) as a basis for an operative guideline]}}. {Epidemiol Prev};2016 (Mar-Apr);40(2 Suppl 1):49-52.
People with autism, their families, and their specialised caregivers are a social group at high health risk after a disruptive earthquake. They need emergency assistance and immediate structured support according to definite protocols and quality standards. We recommend to establish national guidelines for taking-in-charge people with autism after an earthquake. The adaptive behaviour of participants with autism declined dramatically in the first months after the earthquake in all the dimensions examined (i.e., communication, daily living, socialisation, and motor skills). After relatively stable conditions returned and with immediate and intensive post-disaster intervention, children and adolescents with autism showed a trend towards partial recovery of adaptive functioning. As to the impact on services, this study indicates the need for supporting exposed caregivers at high risk of burnout over the first two years after the disaster and for an immediate reorganisation of person-tailored services.
