1. Al-Ayadhi LY, Mostafa GA. {{Elevated serum levels of interleukin-17A in children with autism}}. {J Neuroinflammation}. 2012; 9(1): 158.
ABSTRACT: BACKGROUND: The T-helper (Th)1/Th2 dichotomy dominated the field of immune regulation until interleukin (IL)-17-expressing T cells (Th17) were proposed to be a third lineage of helper T cells, the key players in the pathogenesis of autoimmune disorders. Autoimmunity to brain tissue may play a pathogenic role in autism. IL-17A is a pro-inflammatory cytokine that has been shown to play an important role in various autoimmune neuroinflammatory diseases. The aim of this study was to measure serum levels of IL-17A in relation to the degree of the severity of autism. METHODS: Serum IL-17A levels were measured by ELISA in 45 children with autism and 40 healthy matched healthy controls. RESULTS: Children with autism had significantly higher serum IL-17A levels than healthy controls (P <0.001), with increased serum levels of IL-17A found in 48.9% of the autism group. Patients with severe autism had significantly higher serum IL-17A levels than those with mild to moderate autism (P = 0.01), and raised serum IL-17A levels were significantly more common in children with severe autism (67.9%) than in those with mild to moderate autism (17.6%), P = 0.001. CONCLUSIONS: Serum IL-17A levels were raised in the group with autism, and the levels correlated significantly with the severity of autism. This is the first study to measure levels of IL-17A in relation to the severity of autism, to our knowledge. Further research, with a larger subject population, is warranted to determine whether the increase of serum IL-17A levels plasma has a pathogenic role in autism, and whether anti- IL-17A therapy could be useful.
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2. Angelidou A, Asadi S, Alysandratos KD, Karagkouni A, Kourembanas S, Theoharides TC. {{Perinatal stress, brain inflammation and risk of autism-Review and proposal}}. {BMC Pediatr}. 2012; 12(1): 89.
ABSTRACT: BACKGROUND: Autism Spectrum Disorders (ASD) are neurodevelopmental disorders characterized by varying deficits in social interactions, communication, and learning, as well as stereotypic behaviors. Despite the significant increase in ASD, there are few if any clues for its pathogenesis, hampering early detection or treatment. Premature babies are also more vulnerable to infections and inflammation leading to neurodevelopmental problems and higher risk of developing ASD. Many autism « susceptibility » genes have been identified, but « environmental » factors appear to play a significant role. Increasing evidence suggests that there are different ASD endophenotypes. DISCUSSION: We review relevant literature suggesting in utero inflammation can lead to preterm labor, while insufficient development of the gut-blood-brain barriers could permit exposure to potential neurotoxins. This risk apparently may increase in parents with « allergic » or autoimmune problems during gestation, or if they had been exposed to stressors. The presence of circulating auto-antibodies against fetal brain proteins in mothers is associated with higher risk of autism and suggests disruption of the blood-brain-barrier (BBB). A number of papers have reported increased brain expression or CSF levels of proinflammatory cytokines, especially TNF, which is preformed in mast cells. Recent evidence also indicates increased serum levels of the pro-inflammatory mast cell trigger neurotensin (NT), and of extracellular mitochondrial DNA (mtDNA), which is immunogenic. Mutations of the signal-transduction molecule mTOR and its negative regulator Pten have been linked to autism, but also with proliferation and function of mast cells. SUMMARY: Premature birth and susceptibility genes may make infants more vulnerable to allergic, environmental, infectious, or stress-related triggers that could stimulate mast cell release of pro-inflammatory and neurotoxic molecules, thus contributing to brain inflammation and ASD pathogenesis, at least in an endophenotype of ASD patients.
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3. Carr T, Lord C. {{Longitudinal study of perceived negative impact in African American and Caucasian mothers of children with autism spectrum disorder}}. {Autism}. 2012.
The purpose of this study was to examine the stability of mothers’ perceptions of the negative impact of having a child with ASD in a sample of African American and Caucasian families as their children transitioned to early adolescence. Participants were mothers and children participating in an ongoing longitudinal study of children referred for diagnosis of ASD at age two. Analyses included data from two time points, when child participants were approximately 9 and 14 years old. Linear mixed model analyses were used to examine the relationship between the primary outcome variable, mothers’ perceived negative impact across time, and hypothesized predictors. Negative impact increased significantly from late childhood to into adolescence. However, African American mothers with lower education reported significantly lower levels of perceived negative impact at both time points. Findings show that for some families, the transition to adolescence is a period in which mothers experience increased amounts of negative impact and highlight the importance of examining the influence of socioeconomic variables. Furthermore, data suggest that there may be cultural differences mediating the relationship between maternal education, ethnicity, and perceived negative impact. Implications for the importance of including families from varying levels of socioeconomic status in ASD research are discussed.
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4. Dykstra J, Sabatos-Devito MG, Irvin DW, Boyd BA, Hume KA, Odom SL. {{Using the Language Environment Analysis (LENA) system in preschool classrooms with children with autism spectrum disorders}}. {Autism}. 2012.
This study describes the language environment of preschool programs serving children with autism spectrum disorders (ASDs) and examines relationships between child characteristics and an automated measure of adult and child language in the classroom. The Language Environment Analysis (LENA) system was used with 40 children with ASD to collect data on adult and child language. Standardized assessments were administered to obtain language, cognitive, and autism severity scores for participants. With a mean of over 5 hours of recording across two days several months apart, there was a mean of 3.6 child vocalizations per minute, 1.0 conversational turns (in which either the adult or child respond to the other within 5 seconds) per minute, and 29.2 adult words per minute. Two of the three LENA variables were significantly correlated with language age-equivalents. Cognitive age-equivalents were also significantly correlated with two LENA variables. Autism Diagnostic Observation Schedule severity scores and LENA variables were not significantly correlated. Implications for using the LENA system with children with ASD in the school environment are discussed.
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5. Malesa E, Foss-Feig J, Yoder P, Warren Z, Walden T, Stone W. {{Predicting language and social outcomes at age 5 for later-born siblings of children with autism spectrum disorders}}. {Autism}. 2012.
The relation between early joint attention (in which a child coordinates attention between another person and an object or event) and later language and social outcomes was examined in younger siblings of children with autism spectrum disorder (Sibs-ASD) and younger siblings of children with typical development (Sibs-TD). Initial levels of joint attention (at a mean age of 15 months) as well as growth in levels of joint attention (between 15 months and 34 months) were used as potential predictors of outcomes at age 5. The results revealed that initial levels of initiating joint attention (IJA) were associated with language skills at outcome. In addition, growth of responding to joint attention (RJA) was associated with social skills at age 5. These patterns of associations were not significantly different between the Sibs-TD and Sibs-ASD groups. Although the Sibs-ASD group had lower joint attention scores than the Sibs-TD group at younger ages, significant group differences were not found for most measures at age 5.
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6. Sullivan PF, Magnusson C, Reichenberg A, Boman M, Dalman C, Davidson M, Fruchter E, Hultman CM, Lundberg M, Langstrom N, Weiser M, Svensson AC, Lichtenstein P. {{Family History of Schizophrenia and Bipolar Disorder as Risk Factors for AutismFamily History of Psychosis as Risk Factor for ASD}}. {Arch Gen Psychiatry}. 2012: 1-5.
CONTEXT The clinical and etiologic relation between autism spectrum disorders (ASDs) and schizophrenia is unclear. The degree to which these disorders share a basis in etiology has important implications for clinicians, researchers, and those affected by the disorders. OBJECTIVE To determine whether a family history of schizophrenia and/or bipolar disorder is a risk factor for ASD. DESIGN, SETTING, AND PARTICIPANTS We conducted a case-control evaluation of histories of schizophrenia or bipolar disorder in first-degree relatives of probands in 3 samples-population registers in Sweden, Stockholm County (in Sweden), and Israel. Probands met criteria for ASD, and affection status of parents and siblings for schizophrenia and bipolar disorder were established. RESULTS The presence of schizophrenia in parents was associated with an increased risk for ASD in a Swedish national cohort (odds ratio [OR], 2.9; 95% CI, 2.5-3.4) and a Stockholm County cohort (OR, 2.9; 95% CI, 2.0-4.1). Similarly, schizophrenia in a sibling was associated with an increased risk for ASD in a Swedish national cohort (OR, 2.6; 95% CI, 2.0-3.2) and an Israeli conscription cohort (OR, 12.1; 95% CI, 4.5-32.0). Bipolar disorder showed a similar pattern of associations but of lesser magnitude. CONCLUSIONS Findings from these 3 registers along with consistent findings from a similar study in Denmark suggest that ASD, schizophrenia, and bipolar disorder share common etiologic factors.
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7. Thomas RH, Meeking MM, Mepham JR, Tichenoff L, Possmayer F, Liu S, Macfabe DF. {{The enteric bacterial metabolite propionic acid alters brain and plasma phospholipid molecular species: further development of a rodent model of autism spectrum disorders}}. {J Neuroinflammation}. 2012; 9(1): 153.
ABSTRACT: Gastrointestinal symptoms and altered blood phospholipid profiles have been reported in patients with autism spectrum disorders (ASD). Most of the phospholipid analyses have been conducted on the fatty acid composition of isolated phospholipid classes following hydrolysis. A paucity of information exists on how the intact phospholipid molecular species are altered in ASD. We applied ESI/MS to determine how brain and blood intact phospholipid species were altered during the induction of ASD-like behaviors in rats following intraventricular infusions with the enteric bacterial metabolite propionic acid. Animals were infused daily for 8 days, locomotor activity assessed, and animals killed during the induced behaviors. Propionic acid infusions increased locomotor activity. Lipid analysis revealed treatment altered 21 brain and 30 blood phospholipid molecular species. Notable alterations were observed in the composition of brain SM, diacyl mono and polyunsaturated PC, PI, PS, PE, and plasmalogen PC and PE molecular species. These alterations suggest that the propionic acid rat model is a useful tool to study aberrations in lipid metabolism known to affect membrane fluidity, peroxisomal function, gap junction coupling capacity, signaling, and neuroinflammation, all of which may be associated with the pathogenesis of ASD.
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8. Tillett T. {{A Sensitive Approach to Studying ASDs: Teasing Out Relationships between Autism and Maternal Smoking}}. {Environ Health Perspect}. 2012; 120(7): a285.
