1. {{International society for autism research news}}. {Autism Res};2014 (Apr);7(2):294.
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2. Armstrong A, Knapp VM, McAdam DB. {{Functional analysis and treatment of the diurnal bruxism of a 16-year-old girl with autism}}. {J Appl Behav Anal};2014 (Apr 17)
Bruxism is defined as the clenching and grinding of teeth. This study used a functional analysis to examine whether the bruxism of a 16-year-old girl with autism was maintained by automatic reinforcement or social consequences. A subsequent component analysis of the intervention package described by Barnoy, Najdowski, Tarbox, Wilke, and Nollet (2009) showed that a vocal reprimand (e.g., « stop grinding ») effectively reduced the participant’s bruxism. Results were maintained across time, and effects extended to novel staff members.
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3. Bolte S, Willfors C, Berggren S, Norberg J, Poltrago L, Mevel K, Coco C, Fransson P, Borg J, Sitnikov R, Toro R, Tammimies K, Anderlid BM, Nordgren A, Falk A, Meyer U, Kere J, Landen M, Dalman C, Ronald A, Anckarsater H, Lichtenstein P. {{The Roots of Autism and ADHD Twin Study in Sweden (RATSS)}}. {Twin Res Hum Genet};2014 (Apr 15):1-13.
Neurodevelopmental disorders affect a substantial minority of the general population. Their origins are still largely unknown, but a complex interplay of genetic and environmental factors causing disturbances of the central nervous system’s maturation and a variety of higher cognitive skills is presumed. Only limited research of rather small sample size and narrow scope has been conducted in neurodevelopmental disorders using a twin-differences design. The Roots of Autism and ADHD Twin Study in Sweden (RATSS) is an ongoing project targeting monozygotic twins discordant for categorical or dimensional autistic and inattentive/hyperactive-impulsive phenotypes as well as other neurodevelopmental disorders, and typically developing twin controls. Included pairs are 9 years of age or older, and comprehensively assessed for psychopathology, medical history, neuropsychology, and dysmorphology, as well as structural, functional, and molecular brain imaging. Specimens are collected for induced pluripotent (iPS) and neuroepithelial stem cells, genetic, gut bacteria, protein-/monoamine, and electron microscopy analyses. RATSS’s objective is to generate a launch pad for novel surveys to understand the complexity of genotype-environment-phenotype interactions in autism spectrum disorder and attention-deficit hyperactivity disorder (ADHD). By October 2013, RATSS had collected data from 55 twin pairs, among them 10 monozygotic pairs discordant for autism spectrum disorder, seven for ADHD, and four for other neurodevelopmental disorders. This article describes the design, recruitment, data collection, measures, collected pairs’ characteristics, as well as ongoing and planned analyses in RATSS. Potential gains of the study comprise the identification of environmentally mediated biomarkers, the emergence of candidates for drug development, translational modeling, and new leads for prevention of incapacitating outcomes.
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4. Bonora E, Graziano C, Minopoli F, Bacchelli E, Magini P, Diquigiovanni C, Lomartire S, Bianco F, Vargiolu M, Parchi P, Marasco E, Mantovani V, Rampoldi L, Trudu M, Parmeggiani A, Battaglia A, Mazzone L, Tortora G, Maestrini E, Seri M, Romeo G. {{Maternally inherited genetic variants of CADPS2 are present in Autism Spectrum Disorders and Intellectual Disability patients}}. {EMBO Mol Med};2014 (Apr 14)
Intellectual disability (ID) and autism spectrum disorders (ASDs) are complex neuropsychiatric conditions, with overlapping clinical boundaries in many patients. We identified a novel intragenic deletion of maternal origin in two siblings with mild ID and epilepsy in the CADPS2 gene, encoding for a synaptic protein involved in neurotrophin release and interaction with dopamine receptor type 2 (D2DR). Mutation screening of 223 additional patients (187 with ASD and 36 with ID) identified a missense change of maternal origin disrupting CADPS2/D2DR interaction. CADPS2 allelic expression was tested in blood and different adult human brain regions, revealing that the gene was monoallelically expressed in blood and amygdala, and the expressed allele was the one of maternal origin. Cadps2 gene expression performed in mice at different developmental stages was biallelic in the postnatal and adult stages; however, a monoallelic (maternal) expression was detected in the embryonal stage, suggesting that CADPS2 is subjected to tissue- and temporal-specific regulation in human and mice. We suggest that CADPS2 variants may contribute to ID/ASD development, possibly through a parent-of-origin effect.
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5. Gevarter C, O’Reilly MF, Rojeski L, Sammarco N, Sigafoos J, Lancioni GE, Lang R. {{Comparing Acquisition of AAC-Based Mands in Three Young Children with Autism Spectrum Disorder Using iPad Applications with Different Display and Design Elements}}. {J Autism Dev Disord};2014 (Apr 17)
Augmentative and alternative communication (AAC) applications may differ in their use of display and design elements. Using a multielement design, this study compared mand acquisition in three preschool-aged males with autism spectrum disorder, across three different displays in two iPad(R) AAC applications. Displays included a Widgit symbol button (GoTalk), a photographical hotspot (Scene and Heard), and a Widgit symbol button along with a photograph (Scene and Heard). Applications had additional design differences. Two participants showed more rapid and consistent acquisition with the photographical hotspot than with the symbol button format, but did not master the combined format. The third participant mastered all three conditions at comparable rates. Results suggest that AAC display and design elements may influence mand acquisition.
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6. Greimel E, Schulte-Ruther M, Kamp-Becker I, Remschmidt H, Herpertz-Dahlmann B, Konrad K. {{Impairment in face processing in autism spectrum disorder: a developmental perspective}}. {J Neural Transm};2014 (Apr 16)
Findings on face identity and facial emotion recognition in autism spectrum disorder (ASD) are inconclusive. Moreover, little is known about the developmental trajectory of face processing skills in ASD. Taking a developmental perspective, the aim of this study was to extend previous findings on face processing skills in a sample of adolescents and adults with ASD. N = 38 adolescents and adults (13-49 years) with high-functioning ASD and n = 37 typically developing (TD) control subjects matched for age and IQ participated in the study. Moreover, n = 18 TD children between the ages of 8 and 12 were included to address the question whether face processing skills in ASD follow a delayed developmental pattern. Face processing skills were assessed using computerized tasks of face identity recognition (FR) and identification of facial emotions (IFE). ASD subjects showed impaired performance on several parameters of the FR and IFE task compared to TD control adolescents and adults. Whereas TD adolescents and adults outperformed TD children in both tasks, performance in ASD adolescents and adults was similar to the group of TD children. Within the groups of ASD and control adolescents and adults, no age-related changes in performance were found. Our findings corroborate and extend previous studies showing that ASD is characterised by broad impairments in the ability to process faces. These impairments seem to reflect a developmentally delayed pattern that remains stable throughout adolescence and adulthood.
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7. Hollocks MJ, Jones CR, Pickles A, Baird G, Happe F, Charman T, Simonoff E. {{The association between social cognition and executive functioning and symptoms of anxiety and depression in adolescents with autism spectrum disorders}}. {Autism Res};2014 (Apr);7(2):216-228.
While high levels of anxiety and depression are now recognized as major co-occurring problems in children and young people with an autism spectrum disorder (ASD), research examining possible associations with individual differences in neurocognitive functioning has been limited. This study included 90 adolescents with an ASD aged 14-16 years with a full-scale IQ > 50. Using structural equation modeling, we examined the independent relationships between multiple measures of executive functioning and social cognition on severity of anxiety or depressive symptoms. Results indicated a significant association between poorer executive functioning and higher levels of anxiety, but not depression. In contrast, social cognition ability was not associated with either anxiety or depression. This study is the first to report significant associations between executive functions and anxiety in ASD. This may suggest that poor executive functioning is one factor associated with the high prevalence of anxiety disorder in children and adolescents with ASD. Autism Res 2014, 7: 216-228. (c) 2014 International Society for Autism Research, Wiley Periodicals, Inc.
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8. Isaias IU, Dipaola M, Michi M, Marzegan A, Volkmann J, Rodocanachi Roidi ML, Frigo CA, Cavallari P. {{Gait initiation in children with rett syndrome}}. {PLoS One};2014;9(4):e92736.
Rett syndrome is an X-linked neurodevelopmental condition mainly characterized by loss of spoken language and a regression of purposeful hand use, with the development of distinctive hand stereotypies, and gait abnormalities. Gait initiation is the transition from quiet stance to steady-state condition of walking. The associated motor program seems to be centrally mediated and includes preparatory adjustments prior to any apparent voluntary movement of the lower limbs. Anticipatory postural adjustments contribute to postural stability and to create the propulsive forces necessary to reach steady-state gait at a predefined velocity and may be indicative of the effectiveness of the feedforward control of gait. In this study, we examined anticipatory postural adjustments associated with gait initiation in eleven girls with Rett syndrome and ten healthy subjects. Muscle activity (tibialis anterior and soleus muscles), ground reaction forces and body kinematic were recorded. Children with Rett syndrome showed a distinctive impairment in temporal organization of all phases of the anticipatory postural adjustments. The lack of appropriate temporal scaling resulted in a diminished impulse to move forward, documented by an impairment in several parameters describing the efficiency of gait start: length and velocity of the first step, magnitude and orientation of centre of pressure-centre of mass vector at the instant of (swing-)toe off. These findings were related to an abnormal muscular activation pattern mainly characterized by a disruption of the synergistic activity of antagonistic pairs of postural muscles. This study showed that girls with Rett syndrome lack accurate tuning of feedforward control of gait.
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9. Kobari-Wright VV, Miguel CF. {{The effects of listener training on the emergence of categorization and speaker behavior in children with autism}}. {J Appl Behav Anal};2014 (Apr 17)
We evaluated the effects of listener training on the emergence of categorization and speaker behavior (i.e., tacts) using a nonconcurrent multiple baseline design. Four children with autism learned to select pictures given their dictated category names. We assessed whether they could match and tact pictures by category. After training, 3 participants tacted and categorized all pictures, and 1 participant failed both tests. After tact training, this participant categorized. These results suggest that listener training may be an efficient way to produce speaker behavior and categorization in children who have been diagnosed with autism.
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10. Lin M, Zhao D, Hrabovsky A, Pedrosa E, Zheng D, Lachman HM. {{Heat shock alters the expression of schizophrenia and autism candidate genes in an induced pluripotent stem cell model of the human telencephalon}}. {PLoS One};2014;9(4):e94968.
Schizophrenia (SZ) and autism spectrum disorders (ASD) are highly heritable neuropsychiatric disorders, although environmental factors, such as maternal immune activation (MIA), play a role as well. Cytokines mediate the effects of MIA on neurogenesis and behavior in animal models. However, MIA stimulators can also induce a febrile reaction, which could have independent effects on neurogenesis through heat shock (HS)-regulated cellular stress pathways. However, this has not been well-studied. To help understand the role of fever in MIA, we used a recently described model of human brain development in which induced pluripotent stem cells (iPSCs) differentiate into 3-dimensional neuronal aggregates that resemble a first trimester telencephalon. RNA-seq was carried out on aggregates that were heat shocked at 39 degrees C for 24 hours, along with their control partners maintained at 37 degrees C. 186 genes showed significant differences in expression following HS (p<0.05), including known HS-inducible genes, as expected, as well as those coding for NGFR and a number of SZ and ASD candidates, including SMARCA2, DPP10, ARNT2, AHI1 and ZNF804A. The degree to which the expression of these genes decrease or increase during HS is similar to that found in copy loss and copy gain copy number variants (CNVs), although the effects of HS are likely to be transient. The dramatic effect on the expression of some SZ and ASD genes places HS, and perhaps other cellular stressors, into a common conceptual framework with disease-causing genetic variants. The findings also suggest that some candidate genes that are assumed to have a relatively limited impact on SZ and ASD pathogenesis based on a small number of positive genetic findings, such as SMARCA2 and ARNT2, may in fact have a much more substantial role in these disorders – as targets of common environmental stressors.
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11. Loughrey TO, Betz AM, Majdalany LM, Nicholson K. {{Using instructive feedback to teach category names to children with autism}}. {J Appl Behav Anal};2014 (Apr 17)
We evaluated the effects of instructive feedback (IF) on the emergence of spoken category names with 2 children who had been diagnosed with autism. IF stimuli were presented during listener discrimination training and consisted of presenting the category name associated with each target stimulus. Results suggest that participants acquired the speaker relations in the absence of prompting and reinforcement. Clinical implications and future research on the use of IF as a teaching procedure for children with autism are discussed.
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12. Magid-Bernstein J, Mahajan K, Lincoln J, Ming X, Rohowsky-Kochan C. {{Case Report: Cytokine and CD4+ T-Cell Profiles of Monozygotic Twins With Autism and Divergent Comorbidities and Drug Treatment}}. {J Child Neurol};2014 (Apr 15)
Autism spectrum disorders are neurodevelopmental disorders that are thought to be caused by a gene-by-environment interaction and in which various immune alterations are reported. We investigate CD4+ T-cell cytokine profiles and subpopulations in 19-year-old monozygotic twins with autism and different comorbidities. CD4+ T cells from the twin with epilepsy produce more interferon-gamma, less interleukin-17, and have an increased interferon-gamma/interleukin-4 ratio. CD4+ T cells from the twin with multiple sclerosis exhibit a cytokine profile similar to an age and gender-matched control and a higher percentage of T regulatory (Treg) cells. The twins’ mother’s T cells produce very high levels of both interleukin-17 and interferon-gamma. Cytokine and CD4+ T-cell abnormalities in the twins could contribute to or be a result of the manifestation of their divergent comorbidities. A proinflammatory, autoimmune-polarized cytokine profile is observed in this unique family with autism.
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13. Micheau J, Vimeney A, Normand E, Mulle C, Riedel G. {{Impaired hippocampus-dependent spatial flexibility and sociability represent autism-like phenotypes in GluK2 mice}}. {Hippocampus};2014 (Apr 17)
Autism is a complex neurodevelopmental disorder with high heritability. grik2 (which encodes the GluK2 subunit of kainate receptors) has been identified as a susceptibility gene in Autism Spectrum Disorders (ASD), but its role in the core- and associated-symptoms of ASD still remains elusive.We used mice lacking GluK2 (GluK2 KO) to examine their endophenotype with a view to modeling aspects of autism, including social deficits, stereotyped and repetitive behaviour and decreased cognitive abilities. Anxiety was recorded in the elevated plus maze, social behaviour in a 3-chamber apparatus, and cognition in different water maze protocols. Deletion of the GluK2 gene reduced locomotor activity and sociability as indicated by the social interaction task. In addition, GluK2 KO mice learnt to locate a hidden platform in a water maze surrounded by a curtain with hanging cues faster than wild-type mice. They maintained a bias toward the target quadrant when some of these cues were removed, at which point wild-types orthogonalized the behaviour and showed no memory. However, GluK2 KO mice were impaired in spatial reversal learning. These behavioural data together with previously published electrophysiology showing severe anomalies in CA3 network activity, suggest a computational shift in this network for enhanced propensity of pattern completion that would explain the loss of behavioural flexibility in GluK2 KO mice. Although a single mutation cannot recapitulate the entire core symptoms of ASD, our data provide evidence for glutamatergic dysfunction underlying a number of social- and cognition-related phenotypes relevant to ASD. (c) 2014 Wiley Periodicals, Inc.
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14. Olu-Lafe O, Liederman J, Tager-Flusberg H. {{Is the Ability to Integrate Parts into Wholes Affected in Autism Spectrum Disorder?}}. {J Autism Dev Disord};2014 (Apr 16)
There is considerable debate about whether people with autism spectrum disorder (ASD) are biased toward local information and whether this disrupts their ability to integrate two complex shapes elements into a single figure. Moreover, few have examined the relationship between integration ability and ASD symptom severity. Adolescent/adult males with ASD and age and IQ-matched controls were compared on their performance of a simple silhouette-to-shape matching task and a higher-order shape-integration task. Relative to basic silhouette-to-shape matching, ASD participants were disproportionately slower than controls on shape-integration. Moreover, this relative slowing correlated with increased symptom severity in ASD participants. These findings support the notion that integrating local information is disproportionately more challenging in ASD; this weakness may play a role in ASD symptomatology.
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15. Romano D, Nicolau M, Quintin EM, Mazaika PK, Lightbody AA, Cody Hazlett H, Piven J, Carlsson G, Reiss AL. {{Topological methods reveal high and low functioning neuro-phenotypes within fragile X syndrome}}. {Hum Brain Mapp};2014 (Apr 15)
Fragile X syndrome (FXS), due to mutations of the FMR1 gene, is the most common known inherited cause of developmental disability as well as the most common single-gene risk factor for autism. Our goal was to examine variation in brain structure in FXS with topological data analysis (TDA), and to assess how such variation is associated with measures of IQ and autism-related behaviors. To this end, we analyzed imaging and behavioral data from young boys (n = 52; aged 1.57-4.15 years) diagnosed with FXS. Application of topological methods to structural MRI data revealed two large subgroups within the study population. Comparison of these subgroups showed significant between-subgroup neuroanatomical differences similar to those previously reported to distinguish children with FXS from typically developing controls (e.g., enlarged caudate). In addition to neuroanatomy, the groups showed significant differences in IQ and autism severity scores. These results suggest that despite arising from a single gene mutation, FXS may encompass two biologically, and clinically separable phenotypes. In addition, these findings underscore the potential of TDA as a powerful tool in the search for biological phenotypes of neuropsychiatric disorders. Hum Brain Mapp, 2014. (c) 2014 Wiley Periodicals, Inc.
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16. Siniscalco D, Bradstreet JJ, Cirillo A, Antonucci N. {{The in vitro GcMAF effects on endocannabinoid system transcriptionomics, receptor formation, and cell activity of autism-derived macrophages}}. {J Neuroinflammation};2014 (Apr 17);11(1):78.
BACKGROUND: Immune system dysregulation is well-recognized in autism and thought to be part of the etiology of this disorder. The endocannabinoid system is a key regulator of the immune system via the cannabinoid receptor type 2 (CB2R) which is highly expressed on macrophages and microglial cells. We have previously published significant differences in peripheral blood mononuclear cell CB2R gene expression in the autism population. The use of the Gc protein-derived Macrophage Activating Factor (GcMAF), an endogenous glycosylated vitamin D binding protein responsible for macrophage cell activation has demonstrated positive effects in the treatment of autistic children. In this current study, we investigated the in vitro effects of GcMAF treatment on the endocannabinoid system gene expression, as well as cellular activation in blood monocyte-derived macrophages (BMDMs) from autistic patients compared to age-matched healthy developing controls. METHODS: To achieve these goals, we used biomolecular, biochemical and immunocytochemical methods. RESULTS: GcMAF treatment was able to normalize the observed differences in dysregulated gene expression of the endocannabinoid system of the autism group. GcMAF also down-regulated the over-activation of BMDMs from autistic children. CONCLUSIONS: This study presents the first observations of GcMAF effects on the transcriptionomics of the endocannabinoid system and expression of CB2R protein. These data point to a potential nexus between endocannabinoids, vitamin D and its transporter proteins, and the immune dysregulations observed with autism.
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17. Smith RM, Banks W, Hansen E, Sadee W, Herman GE. {{Family-Based Clinical Associations and Functional Characterization of the Serotonin 2A Receptor Gene (HTR2A) in Autism Spectrum Disorder}}. {Autism Res};2014 (Apr 17)
The serotonin 2A receptor gene (HTR2A) harbors two functional single nucleotide polymorphisms (SNPs) that are frequent in populations of African and European descent; rs6311, which affects mRNA expression, and rs6314, which changes the amino acid sequence of the encoded protein and affects the signaling properties of the receptor. Multiple clinical associations support a role for these SNPs in cognitive and neuropsychiatric phenotypes, although studies in autism spectrum disorder (ASD) remain equivocal. Here, we tested transmission disequilibrium of rs6311 and rs6314 in a cohort of 158 ASD trios (simplex and multiplex), observing significant under-transmission of the minor « A » allele of rs6311 to offspring with ASD (permuted P = 0.0004). Consistent with our previous findings in the dorsolateral prefrontal cortex of unaffected individuals, rs6311/A decreases expression of HTR2A mRNA with an extended 5′ untranslated region (UTR) in the frontopolar cortex in brain samples from 54 ASD patients and controls. Interpreting the clinical results in the context of our mRNA expression analysis, we speculate that any risk associated with rs6311 is conferred by greater expression of the long 5’UTR mRNA isoform. The current study corroborates earlier associations between rs6311 and ASD in a family study, supporting the hypothesis that rs6311 plays a modulatory role in ASD risk. Autism Res 2014, : -. (c) 2014 International Society for Autism Research, Wiley Periodicals, Inc.
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18. Steiner NJ, Frenette E, Hynes C, Pisarik E, Tomasetti K, Perrin EC, Rene K. {{A Pilot Feasibility Study of Neurofeedback for Children with Autism}}. {Appl Psychophysiol Biofeedback};2014 (Apr 16)
Neurofeedback (NFB) is an emerging treatment for children with autism spectrum disorder (ASD). This pilot study examined the feasibility of NFB for children with ASD. Ten children ages 7-12 with high functioning ASD and attention difficulties received a NFB attention training intervention. A standardized checklist captured feasibility, including focus during exercises and academic tasks, as well as off-task behaviors. Active behaviors and vocalizations were the most frequent off-task behaviors. Positive reinforcement and breaks including calm breathing exercises were the most common supports. Low motivation was associated with higher feasibility challenges, yet parental involvement and accommodations were helpful. This pilot study shows that it is feasible to conduct NFB sessions with children with high functioning autism and attention difficulties.
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19. Vivanti G, Trembath D, Dissanayake C. {{Mechanisms of Imitation Impairment in Autism Spectrum Disorder}}. {J Abnorm Child Psychol};2014 (Apr 16)
Individuals with Autism Spectrum Disorders (ASD) have difficulties with imitation, though the nature of these remains unclear. In this study, involving 28 preschoolers with ASD (M age = 48 months; 90 % male), 17 matched children with Global Developmental Delay (GDD group; M age = 44 months; 53 % male) and 17 typically developing children (TD group, M age = 52 months; 65 % male), we found that preschoolers with ASD 1) imitate less frequently than both typically developing children and children with GDD; 2) when they do imitate, their imitation is less accurate than that of TD children but similar to that of children with GDD; 3) unlike participants in both comparison groups, preschoolers with ASD use emulation more often than imitation when copying others’ actions; 4) they spend less time looking at the model’s face and more time looking at her actions; and 5) attentional, social and executive factors underlie different aspects of imitation difficulties in this population. Implications for developmental models of autism are discussed.
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20. Wang Y, Fang Y, Zhang F, Xu M, Zhang J, Yan J, Ju W, Brown WT, Zhong N. {{Hypermethylation of the enolase gene (ENO2) in autism}}. {Eur J Pediatr};2014 (Apr 17)
It has been hypothesized that dysregulation of brain-expressed genes is the major predisposing underlying mechanism for autism. This dysregulation may be mediated by differential methylation of CpG sites within gene promoters, which could be candidate biomarkers and used for early clinical screening of autism. A total of 131 pairs of age- and sex-matched autistic and control subjects were recruited in this study. Peripheral blood cells were analyzed. The first five pairs were randomly applied to array-based genome-wide methylation studies. A neuron-specific gene, ENO2, was found to be hypermethylated in the autistic samples. This difference was validated by bisulfite sequencing PCR (BSP). The differential expression of ENO2 gene was further analyzed with RT-qPCR and ELISA. The hypermethylation of ENO2 within the promoter region was confirmed by BSP to be present in 14.5 % (19/131) of the total of the autistic samples. The mean ENO2 RNA level in these 19 autistic samples was reduced by about 70 % relative to that in controls. The average level of ENO2 protein expression in the 19 autistic samples (15.18 +/- 3.51 mug/l) was about half of that in the controls (33.86 +/- 8.16 mug/l). Conclusion: These findings suggest that reduced ENO2 expression may be a biomarker for a subset of autistic children.
