1. Allen NM, Conroy J, Deonna T, McCreary D, McGettigan P, Madigan C, Carter I, Ennis S, Lynch SA, Shahwan A, King MD. {{Atypical benign partial epilepsy of childhood with acquired neurocognitive, lexical semantic, and autistic spectrum disorder}}. {Epilepsy Behav Case Rep};2016;6:42-48.
Atypical benign partial epilepsy (ABPE) of childhood or pseudo-Lennox syndrome is a form of idiopathic focal epilepsy characterized by multiple seizure types, focal and/or generalized epileptiform discharges, continuous spike-wave during sleep (CSWS), and sometimes reversible neurocognitive deficits. There are few reported cases of ABPE describing detailed correlative longitudinal follow-up of the various associated neurocognitive, language, social communicative, or motor deficits, in parallel with the epilepsy. Furthermore, the molecular inheritance pattern for ABPE and the wider spectrum of epilepsy aphasia disorders have yet to be fully elucidated. We describe the phenotype-genotype study of a boy with ABPE with follow-up from ages 5 to 13 years showing acquired oromotor and, later, a specific lexical semantic and pervasive developmental disorder. Exome sequencing identified variants in SCN9A, CPA6, and SCNM1. A direct role of the epilepsy in the pathogenesis of the oromotor and neurocognitive deficits is apparent.
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2. Armeanu R, Mokkonen M, Crespi B. {{Meta-Analysis of BDNF Levels in Autism}}. {Cell Mol Neurobiol};2016 (Aug 8)
Brain-derived neurotrophic factor (BDNF) centrally mediates growth, differentiation and survival of neurons, and the synaptic plasticity that underlies learning and memory. Recent meta-analyses have reported significantly lower peripheral BDNF among individuals with schizophrenia, bipolar disorder, and depression, compared with controls. To evaluate the role of BDNF in autism, and to compare autism to psychotic-affective disorders with regard to BDNF, we conducted a meta-analysis of BDNF levels in autism. Inclusion criteria were met by 15 studies, which included 1242 participants. The meta-analysis estimated a significant summary effect size of 0.33 (95 % CI 0.21-0.45, P < 0.001), suggesting higher BDNF in autism than in controls. The studies showed notable heterogeneity, but no evidence of publication biases. Higher peripheral BDNF in autism is concordant with several neurological and psychological theories on the causes and symptoms of this condition, and it contrasts notably with the lower levels of BDNF found in schizophrenia, bipolar disorder, and depression. Lien vers le texte intégral (Open Access ou abonnement)
3. Aydin HI. {{Genetic Studies in Autism: Correspondence}}. {Indian J Pediatr};2016 (Aug 10)
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4. Bodaleo FJ, Gonzalez-Billault C. {{The Presynaptic Microtubule Cytoskeleton in Physiological and Pathological Conditions: Lessons from Drosophila Fragile X Syndrome and Hereditary Spastic Paraplegias}}. {Front Mol Neurosci};2016;9:60.
The capacity of the nervous system to generate neuronal networks relies on the establishment and maintenance of synaptic contacts. Synapses are composed of functionally different presynaptic and postsynaptic compartments. An appropriate synaptic architecture is required to provide the structural basis that supports synaptic transmission, a process involving changes in cytoskeletal dynamics. Actin microfilaments are the main cytoskeletal components present at both presynaptic and postsynaptic terminals in glutamatergic synapses. However, in the last few years it has been demonstrated that microtubules (MTs) transiently invade dendritic spines, promoting their maturation. Nevertheless, the presence and functions of MTs at the presynaptic site are still a matter of debate. Early electron microscopy (EM) studies revealed that MTs are present in the presynaptic terminals of the central nervous system (CNS) where they interact with synaptic vesicles (SVs) and reach the active zone. These observations have been reproduced by several EM protocols; however, there is empirical heterogeneity in detecting presynaptic MTs, since they appear to be both labile and unstable. Moreover, increasing evidence derived from studies in the fruit fly neuromuscular junction proposes different roles for MTs in regulating presynaptic function in physiological and pathological conditions. In this review, we summarize the main findings that support the presence and roles of MTs at presynaptic terminals, integrating descriptive and biochemical analyses, and studies performed in invertebrate genetic models.
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5. Burkett K, Morris E, Anthony J, Shambley-Ebron D, Manning-Courtney P. {{Parenting African American Children With Autism: The Influence of Respect and Faith in Mother, Father, Single-, and Two-Parent Care}}. {J Transcult Nurs};2016 (Aug 10)
PURPOSE: Parents are the most significant contributor to care of children with autism spectrum disorder (ASD), and as such research on African American parenting in ASD is conspicuously absent. Findings relevant to parenting are discussed from a study with urban African American families caring for children with ASD. DESIGN: An ethnonursing study was conducted with 24 African American family members of children with ASD and 28 professionals. Data were analyzed and reported as themes. FINDINGS: Two universal themes of were found of respect and faith in God and family that influenced parental care. Two diverse themes of mother’s watchful care and father’s protective care, along with differences in feelings of isolation and dependence on supports were found among single- and two-parent families. DISCUSSION AND PRACTICE IMPLICATIONS: When health care professionals increase their knowledge and understanding of cultural practices in the parental care of children with ASD, they provide health care that is culturally congruent.
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6. Chesnut SR, Wei T, Barnard-Brak L, Richman DM. {{A meta-analysis of the social communication questionnaire: Screening for autism spectrum disorder}}. {Autism};2016 (Aug 7)
The current meta-analysis examines the previous research on the utility of the Social Communication Questionnaire as a screening instrument for autism spectrum disorder. Previously published reports have highlighted the inconsistencies between Social Communication Questionnaire-screening results and formal autism spectrum disorder diagnoses. The variations in accuracy resulted in some researchers questioning the validity of the Social Communication Questionnaire. This study systematically examined the accuracy of the Social Communication Questionnaire as a function of the methodological decisions made by researchers screening for autism spectrum disorder over the last 15 years. Findings from this study suggest that the Social Communication Questionnaire is an acceptable screening instrument for autism spectrum disorder (area under the curve = 0.885). Variations in methodological decisions, however, greatly influenced the accuracy of the Social Communication Questionnaire in screening for autism spectrum disorder. Of these methodological variations, using the Current instead of the Lifetime version of the Social Communication Questionnaire resulted in the largest detrimental effect (d = -3.898), followed by using the Social Communication Questionnaire with individuals younger than 4 years of age (d = -2.924) and relying upon convenience samples (d = -4.828 for clinical samples, -2.734 for convenience samples, and -1.422 for community samples). Directions for future research and implications for using the Social Communication Questionnaire to screen for autism spectrum disorder are discussed.
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7. Durbin A, Sirotich F, Lunsky Y, Roesslein K, Durbin J. {{Needs among persons with human immunodeficiency virus and intellectual and developmental disabilities in community mental health care: a cross-sectional study}}. {J Intellect Disabil Res};2016 (Aug 10)
BACKGROUND: The experience of having human immunodeficiency virus (HIV) is often associated with co-occurring mental health issues. Community mental health services are an important source of support for persons with HIV living in the community. Persons with intellectual disability (ID) are vulnerable to HIV and may have unique support needs beyond those without ID receiving community care. This study compared support needs of men with HIV in community mental health programmes, with and without ID. METHODS: The sample was composed of 138 HIV-positive men with and without ID receiving mental health case management from one community organisation in Ontario, Canada, on 31 March 2013. Staff-rated needs across 16 domains grouped into four clusters were measured using the Camberwell Assessment of Need: Basic needs (accommodation, food, public transportation, money and benefits); self-care/functional needs (looking after the home, self-care and daytime activities); health/safety needs (physical health, psychological distress, psychotic symptoms, safety to self and safety to others); and social needs (company, intimate relationships and sexual expression). Adjusted logistic regression models examined the association between ID and each need domain. RESULTS: One-quarter of the sample (n = 34/138, 24.6%) had co-occurring ID. Those with ID were more likely to have needs in the basic cluster [odds ratios: food 4.05 (1.14, 14.44), P:0.031; benefits 2.58 (1.05, 6.32), P:0.038)] and self-care/functional cluster [looking after the home (2.75 (1.17, 6.49), P:0.021); self-care (2.72 (1.18, 6.27), P:0.019)], but were less likely to have need for sexual expression: 0.35 (0.14,0.90), P:0.030) (social cluster). There were no differences in the domains in the health/safety cluster. CONCLUSION: Despite elevated cognitive needs in the basic and self-care/functional clusters for the ID group, limited other differences suggest that with moderate additional targeting, community mental health programmes for persons with HIV may be appropriate for men with ID.
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8. Frazier TW, Hardan AY. {{Equivalence of symptom dimensions in females and males with autism}}. {Autism};2016 (Aug 7)
This study investigated equivalence of autism symptom domains in males and females with autism. Symptom data were obtained from 2643 children and adolescents with autism spectrum disorder (352 females, 2291 males; age range = 4-17 years) included in the Simons Simplex Collection. Items from the Social Responsiveness Scale and Autism Diagnostic Interview-Revised were mapped to nine a priori symptom dimensions. Multi-group confirmatory factor models, including measurement equivalence and item response theory analyses, examined whether males and females showed measurement or structural differences in autism symptom constructs. Results indicated mean differences in restricted interests that were not due to measurement bias. No other symptom dimension showed evidence of measurement bias and autism symptom structure was highly similar between males and females. Future studies are needed to carefully estimate any sex differences in the content, frequency, or intensity/severity of restricted interests in females and males.
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9. Howard PL, Liversedge SP, Benson V. {{Benchmark Eye Movement Effects During Natural Reading in Autism Spectrum Disorder}}. {J Exp Psychol Learn Mem Cogn};2016 (Aug 8)
In 2 experiments, eye tracking methodology was used to assess on-line lexical, syntactic and semantic processing in autism spectrum disorder (ASD). In Experiment 1, lexical identification was examined by manipulating the frequency of target words. Both typically developed (TD) and ASD readers showed normal frequency effects, suggesting that the processes TD and ASD readers engage in to identify words are comparable. In Experiment 2, syntactic parsing and semantic interpretation requiring the on-line use of world knowledge were examined, by having participants read garden path sentences containing an ambiguous prepositional phrase. Both groups showed normal garden path effects when reading low-attached sentences and the time course of reading disruption was comparable between groups. This suggests that not only do ASD readers hold similar syntactic preferences to TD readers, but also that they use world knowledge on-line during reading. Together, these experiments demonstrate that the initial construction of sentence interpretation appears to be intact in ASD. However, the finding that ASD readers skip target words less often in Experiment 2, and take longer to read sentences during second pass for both experiments, suggests that they adopt a more cautious reading strategy and take longer to evaluate their sentence interpretation prior to making a manual response. (PsycINFO Database Record
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10. Hundley RJ, Shui A, Malow BA. {{Relationship Between Subtypes of Restricted and Repetitive Behaviors and Sleep Disturbance in Autism Spectrum Disorder}}. {J Autism Dev Disord};2016 (Aug 10)
We examined the association of two types of restricted and repetitive behaviors, repetitive sensory motor (RSM) and insistence on sameness (IS), with sleep problems in children with autism spectrum disorder (ASD). Participants included 532 children (aged 2-17) who participated in the Autism Speaks Autism Treatment Network research registry. Confirmatory factor analysis of the Autism Diagnostic Interview-Revised detected the presence of RSM and IS. RSM behaviors were positively associated with parent-reported sleep problems, and this relationship remained significant after controlling for anxiety symptoms. IS was not significantly associated with sleep problems. Better understanding of the relationship between specific types of repetitive behaviors and sleep problems may allow providers to tailor interventions to the individual presentations of their patients with ASD.
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11. Inoue YU, Inoue T. {{Brain enhancer activities at the gene-poor 5p14.1 autism-associated locus}}. {Sci Rep};2016;6:31227.
Due to the vast clinical and genetic heterogeneity, identification of causal genetic determinants for autism spectrum disorder (ASD) has proven to be complex. Whereas several dozen ‘rare’ genetic variants for ASD susceptibility have been identified, studies are still underpowered to analyse ‘common’ variants for their subtle effects. A recent application of genome-wide association studies (GWAS) to ASD indicated significant associations with the single nucleotide polymorphisms (SNPs) on chromosome 5p14.1, located in a non-coding region between cadherin10 (CDH10) and cadherin9 (CDH9). Here we apply an in vivo bacterial artificial chromosome (BAC) based enhancer-trapping strategy in mice to scan the gene desert for spatiotemporal cis-regulatory activities. Our results show that the ASD-associated interval harbors the cortical area, striatum, and cerebellum specific enhancers for a long non-coding RNA, moesin pseudogene1 antisense (MSNP1AS) during the brain developing stages. Mouse moesin protein levels are not affected by exogenously expressed human antisense RNAs in our transgenic brains, demonstrating the difficulty in modeling rather smaller effects of common variants. Our first in vivo evidence for the spatiotemporal transcription of MSNP1AS however provides a further support to connect this intergenic variant with the ASD susceptibility.
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12. Jackson JL. {{Capsule Commentary on Nicolaidis et al., The Development and Evaluation of an Online Healthcare Toolkit for Autistic Adults and their Primary Care Providers}}. {J Gen Intern Med};2016 (Aug 10)
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13. Kirby AV, Baranek GT, Fox L. {{Longitudinal Predictors of Outcomes for Adults With Autism Spectrum Disorder: Systematic Review}}. {OTJR (Thorofare N J)};2016 (Apr);36(2):55-64.
To generate an evidence-based understanding of longitudinal predictors of social outcomes (i.e., employment, social relationships/participation, independent living) of adults with autism spectrum disorder (ASD), we conducted a systematic literature review of publications since 2000. Twelve publications deriving from eight study samples fit inclusion/exclusion criteria for the review. In these publications, statistically significant predictors of social outcomes fell into five categories: (a) personal characteristics, (b) individual functioning, (c) family context, (d) services, and (e) other factors (i.e., peer influence, health status). However, only two studies demonstrated high methodological quality, and only one category of predictors-individual functioning-was identified across multiple study samples. To inform practices for youth with ASD, there remains a need for high-quality outcome research related to adults with ASD to better understand predictors, especially related to environmental factors such as related to the family and services received.
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14. Kosaki Y, Watanabe S. {{Impaired Pavlovian predictive learning between temporally phasic but not static events in autism-model strain mice}}. {Neurobiol Learn Mem};2016 (Aug 10)
Autism-spectrum disorder (ASD) is a multi-aspect developmental disorder characterised by various social and non-social behavioural abnormalities. Using BTBR T+ tf mouse strain (BTBR), a promising animal model displaying a number of behavioural and neural characteristics associated with ASD, we tested the hypothesis that at the core of various symptoms of ASD lies a fundamental deficit in predictive learning between events. In five experiments, we conducted a variety of Pavlovian conditioning tasks, some requiring the establishment of associations between temporally phasic events and others involving static events. BTBR mice were impaired in the acquisition of conditioned magazine approach responses with an appetitive unconditioned stimulus (US) (Experiment 1) and conditioned freezing with an electric shock US (Experiment 2). Both of these tasks had temporally phasic conditioned stimuli (CSs). Conversely, these mice showed normal acquisition of conditioned place preference (CPP), whether the US was a systemic injection of methamphetamine (Experiment 3A) or the presence of food (Experiment 3B). Experiment 4 showed normal acquisition of conditioned taste aversion (CTA) to a flavour-taste compound CS, although BTBR mice still exhibited an abnormal stimulus selection when learning for each element of the compound CS was assessed separately. Experiment 5 revealed a weaker latent inhibition of CTA in BTBR mice. The BTBR mouse’s impaired predictive learning between phasic events and intact associations between static events are discussed in terms of dysfunctional contingency-based, but not contiguity-based learning, which may accompany abnormal selective attention to relevant cues. We propose that such dysfunctional contingency learning mechanisms may underlie the development of various social and non-social symptoms of ASD.
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15. Oxelgren UW, Myrelid A, Anneren G, Ekstam B, Goransson C, Holmbom A, Isaksson A, Aberg M, Gustafsson J, Fernell E. {{Prevalence of autism and attention-deficit-hyperactivity disorder in Down syndrome: a population-based study}}. {Dev Med Child Neurol};2016 (Aug 9)
AIM: To investigate the prevalence of autism spectrum disorder (ASD) and attention-deficit-hyperactivity disorder (ADHD) in a population-based group of children and adolescents with Down syndrome, and to relate the findings to level of intellectual disability and to medical conditions. METHOD: From a population-based cohort of 60 children and adolescents with Down syndrome, 41 individuals (29 males, 12 females; mean age 11y, age range 5-17y) for whom parents gave consent for participation were clinically assessed with regard to ASD and ADHD. The main instruments used were the Autism Diagnostic Interview-Revised, Autism Diagnostic Observation Schedule, Swanson, Nolan, and Pelham-IV Rating Scale, and the Adaptive Behavior Assessment System-II. RESULTS: High rates of ASD and ADHD were found: 17 (42%) and 14 (34%) of the 41 children met DSM criteria for ASD and ADHD respectively. INTERPRETATION: Children with Down syndrome and coexisting neurodevelopmental/neuropsychiatric disorders in addition to intellectual disability and medical disorders constitute a severely disabled group. Based on the results, we suggest that screening is implemented for both ASD and ADHD, at the age of 3 to 5 years and early school years respectively, to make adequate interventions possible.
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16. Singer AB, Windham GC, Croen LA, Daniels JL, Lee BK, Qian Y, Schendel DE, Fallin MD, Burstyn I. {{Maternal Exposure to Occupational Asthmagens During Pregnancy and Autism Spectrum Disorder in the Study to Explore Early Development}}. {J Autism Dev Disord};2016 (Aug 10)
Maternal immune activity has been linked to children with autism spectrum disorder (ASD). We examined maternal occupational exposure to asthma-causing agents during pregnancy in relation to ASD risk. Our sample included 463 ASD cases and 710 general population controls from the Study to Explore Early Development whose mothers reported at least one job during pregnancy. Asthmagen exposure was estimated from a published job-exposure matrix. The adjusted odds ratio for ASD comparing asthmagen-exposed to unexposed was 1.39 (95 % CI 0.96-2.02). Maternal workplace asthmagen exposure was not associated with ASD risk in this study, but this result does not exclude some involvement of maternal exposure to asthma-causing agents in ASD.
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17. Somekh J, Peleg M, Eran A, Koren I, Feiglin A, Demishtein A, Shiloh R, Heiner M, Kong SW, Elazar Z, Kohane I. {{A Model-driven methodology for exploring complex disease comorbidities applied to autism spectrum disorder and inflammatory bowel disease}}. {J Biomed Inform};2016 (Aug 10)
We propose a model-driven methodology aimed to shed light on complex disorders. Our approach enables exploring shared etiologies of comorbid diseases at the molecular pathway level. The method, Comparative Comorbidities Simulation (CCS), uses stochastic Petri net simulation for examining the phenotypic effects of perturbation of a network known to be involved in comorbidities to predict new roles for mutations in comorbid conditions. To demonstrate the utility of our novel methodology, we investigated the molecular convergence of autism spectrum disorder (ASD) and inflammatory bowel disease (IBD) on the autophagy pathway. In addition to validation by domain experts, we used formal analyses to demonstrate the model’s self-consistency. We then used CCS to compare the effects of loss of function (LoF) mutations previously implicated in either ASD or IBD on the autophagy pathway. CCS identified similar dynamic consequences of these mutations in the autophagy pathway. Our method suggests that two LoF mutations previously implicated in IBD may contribute to ASD, and one ASD-implicated LoF mutation may play a role in IBD. Future targeted genomic or functional studies could be designed to directly test these predictions.
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18. Takarae Y, Sablich SR, White SP, Sweeney JA. {{Neurophysiological hyperresponsivity to sensory input in autism spectrum disorders}}. {J Neurodev Disord};2016;8:29.
BACKGROUND: Atypical sensory processing is a common clinical observation in autism spectrum disorder (ASD). Neural hyperexcitability has been suggested as the cause for sensory hypersensitivity, a frequently reported clinical observation in ASD. We examined visual evoked responses to parametric increases in stimulus contrast in order to model neural responsivity of sensory systems in ASD. METHODS: Thirteen high-functioning individuals with ASD and 12 typically developing (TD) individuals completed a steady-state visual evoked potential study. Stimuli were vertical circular gratings oscillating at 3.76 Hz at varying contrasts (5, 10, 20,…, 90 % contrast, 10 levels). The average spectral power at the stimulus oscillation frequency was calculated for each contrast level. RESULTS: The magnitude of evoked sensory responses increased at a significantly greater rate and resulted in disproportionately elevated activation with higher contrasts in the ASD group. Approximately 45 % of ASD participants had rates of response increases greater than any TD participant. This alteration was highly associated with parental reports of these participants’ sensory difficulties. CONCLUSIONS: Greater increases in visual responses over contrast manipulation suggest heightened excitability in the sensory cortex in ASD participants. Heightened neural excitability was observed in a substantial portion but not all of the ASD participants. This pattern suggests that individuals with higher excitability may constitute a neurobiologically distinct subgroup requiring individualized treatment interventions.
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19. Truszkowski TL, James EJ, Hasan M, Wishard TJ, Liu Z, Pratt KG, Cline HT, Aizenman CD. {{Fragile X mental retardation protein knockdown in the developing Xenopus tadpole optic tectum results in enhanced feedforward inhibition and behavioral deficits}}. {Neural Dev};2016;11(1):14.
BACKGROUND: Fragile X Syndrome is the leading monogenetic cause of autism and most common form of intellectual disability. Previous studies have implicated changes in dendritic spine architecture as the primary result of loss of Fragile X Mental Retardation Protein (FMRP), but recent work has shown that neural proliferation is decreased and cell death is increased with either loss of FMRP or overexpression of FMRP. The purpose of this study was to investigate the effects of loss of FMRP on behavior and cellular activity. METHODS: We knocked down FMRP expression using morpholino oligos in the optic tectum of Xenopus laevis tadpoles and performed a series of behavioral and electrophysiological assays. We investigated visually guided collision avoidance, schooling, and seizure propensity. Using single cell electrophysiology, we assessed intrinsic excitability and synaptic connectivity of tectal neurons. RESULTS: We found that FMRP knockdown results in decreased swimming speed, reduced schooling behavior and decreased seizure severity. In single cells, we found increased inhibition relative to excitation in response to sensory input. CONCLUSIONS: Our results indicate that the electrophysiological development of single cells in the absence of FMRP is largely unaffected despite the large neural proliferation defect. The changes in behavior are consistent with an increase in inhibition, which could be due to either changes in cell number or altered inhibitory drive, and indicate that FMRP can play a significant role in neural development much earlier than previously thought.
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20. Xie J, Li H, Zhu H, Huang L, Zhang X, Zhou Y, Zhou Q, Xu W. {{[Analysis of DIAPH3 gene mutation in a boy with autism spectrum disorder]}}. {Zhonghua Yi Xue Yi Chuan Xue Za Zhi};2016 (Aug 10);33(4):481-484.
OBJECTIVE: To analyze the clinical manifestations and gene mutation of a 6 year old boy with autism spectrum disorders (ASD). METHODS: Peripheral blood of the boy and his parents were subjected to genetic testing. RESULTS: The patient was diagnosed with typical autism. Exome sequencing has identified mutations of four candidate genes, namely TUT1, DIAPH3, REELIN and SETD2, which were confirmed with Sanger sequencing. Analysis of family members confirmed that the missense mutations of DIAPH3 and SETD2 genes were of de novo origin. CONCLUSION: Missense mutations of DIAPH3 and SETD2 genes may have contributed to the risk of ASD. Disrupted neurogenesis associated with such mutations may have been the underlying mechanism for ASD.
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21. Zheng Z, Zhang L, Zhu T, Huang J, Qu Y, Mu D. {{Peripheral brain-derived neurotrophic factor in autism spectrum disorder: a systematic review and meta-analysis}}. {Sci Rep};2016;6:31241.
Brain-derived neurotrophic factor (BDNF) regulates neuronal survival and growth and promotes synaptic plasticity. Recently, researchers have begun to explore the relationship between peripheral BDNF levels and autism spectrum disorder (ASD), but the findings are inconsistent. We undertook the first systematic review and meta-analysis of studies examining peripheral BDNF levels in ASD compared with healthy controls. The PubMed, Embase, and Cochrane Library databases were searched for studies published before February 2016. Fourteen studies involving 2,707 participants and 1,131 incident cases were included. The meta-analysis provided evidence of higher peripheral BDNF levels in ASD compared with controls [standardized mean difference (SMD) = 0.63, 95% confidence interval (95% CI) = 0.18-1.08; P = 0.006]. Subgroup analyses revealed higher BDNF levels in ASD compared with controls for both serum [SMD = 0.58, 95% CI = 0.11-1.04; P = 0.02] and plasma [SMD = 1.27, 95% CI = 0.92-1.61; P < 0.001]. Studies of childhood yielded similar cumulative effect size [SMD = 0.78, 95% CI = 0.31-1.26; P = 0.001], while this was not true for the studies of adulthood [SMD = 0.04, 95% CI = -1.72-1.80; P = 0.97]. This meta-analysis suggests that peripheral BDNF levels are a potential biomarker of ASD. Lien vers le texte intégral (Open Access ou abonnement)