Gut microbiota of patients with autism spectrum disorders
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ABSTRACT:
PROVIDER: PRJEB23052 | ENA |
REPOSITORIES: ENA
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Project description:Here we report metagenomic sequencing data in gut microbiota of autism spectrum disorders (ASD) compared with healthy volunteers (30 for ASD children and 30 for healthy controls, respectively). The genes changed in autistic subjects involved 1,312,364 analytes that compare to 1,335,835 analytes in healthy controls. The number of taxa in autistic subjects were significantly increased as compared to the healthy controls based on the phylum and genus level (P = 0.001). However, the number of species were significantly decreased in autistic subjects (P = 0.001).
2020-09-30 | GSE113540 | GEO
Project description:Here we report 16S rRNA data in gut microbiota of autism spectrum disorders compared with healthy volunteers. A total of 1322 operational taxonomic units (OTUs) were identified in the sequence data. The Bacteroidetes and Firmicutes were both dominated phylum in ausitic subjects and healthy controls. Phylum level analysis showed a clear alteration of the bacterial gut community in ASD characterized by a higher Firmicutes (P < 0.05), Proteobacteria (P < 0.001), and Actinobacteria (P < 0.001) than that in healthy controls. However, Bacteroidetes were significantly decreased in ASD patients (P < 0.001).
2020-09-30 | GSE113690 | GEO
Project description:We transplanted gut microbiota via fecal transfer from TD and ASD children into germ-free wild-type mice, and reveal that colonization with ASD microbiomes induces hallmark changes in sociability, vocalization, and stereotypies. The brains of mice receiving gut microbiota from ASD individuals display alternative splicing patterns for genes dysregulated in the human ASD brain.
2019-02-01 | GSE109827 | GEO
Project description:Autism spectrum disorder (ASD) manifests as alterations in complex human behaviors including social communication and stereotypies. In addition to genetic risks, the gut microbiome differs between typically-developing (TD) and ASD individuals, though it remains unclear whether the microbiome contributes to symptoms. We transplanted gut microbiota from human donors with ASD and TD controls into germ-free mice, and reveal that colonization with ASD microbiota was sufficient to induce hallmark autistic behaviors. The brains of mice colonized with ASD microbiota display alternative splicing of ASD-relevant genes. Microbiome and metabolome profiles of mice harboring human microbiota predict that specific bacterial taxa and their metabolites modulate ASD behaviors. Indeed, treatment of an ASD mouse model with candidate microbial metabolites improves behavioral abnormalities and affects neuronal excitability in the brain. We propose that the gut microbiome modulates behaviors in mice via production of neuroactive metabolites, suggesting that gut-brain connections contribute to the pathophysiology of ASD.
2019-07-04 | MTBLS726 | MetaboLights
Project description:Alterations in the composition of the gut microbiome have an emerging role in brain function and behaviour. We have porposed that short chain fatty acids (SCFA) including propionate and butyrate which are present in the diet and are fermantation products of many gastrointestinal bacteria are contributing environmental factors in autism spectrum disorders (ASD). Here we used the microarray technology to compare global changes in gene expression profiles following exposure of PC12 cells to structurally related SCFA propionate and butyrate each in two different concentrations. Large number of affected genes, common for both SCFA were identified, including genetic networks and GO processes implicated in ASD. PC12 cells were exposed to propionate or butyrate. RNA was isolated from each experimental group (n=6, pooled samples) and subjected to genome-wide expression profiling using Affymetrix microarrays to reveal dose- and SCFA-specific changes in gene expression and specific molecular pathways or processes affected as compared to vehicle treated controls.
2014-06-02 | E-GEOD-56516 | biostudies-arrayexpress
Project description:Autism spectrum disorders (ASD) are neurodevelopmental disorders characterized by delayed/abnormal language development, deficits in social interaction, repetitive behaviors and restricted interests. The heterogeneity in clinical presentation of ASD, likely due to different etiologies, complicates genetic/biological analyses of these disorders. DNA microarray analyses were conducted on 116 lymphoblastoid cell lines (LCL) from individuals with idiopathic autism who are divided into 3 phenotypic subgroups according to severity scores from the commonly used Autism Diagnostic Interview-Revised questionnaire and age-matched, nonautistic controls. Statistical analyses of gene expression data from control LCL against that of LCL from ASD probands identify genes for which expression levels are either quantitatively or qualitatively associated with phenotypic severity. Comparison of the significant differentially expressed genes from each subgroup relative to the control group reveals differentially expressed genes unique to each subgroup as well as genes in common across subgroups. Among the findings unique to the most severely affected ASD group are genes that regulate circadian rhythm, which has been shown to have multiple effects on neurological as well as metabolic functions commonly dysregulated in autism. Among the genes common to all 3 subgroups of ASD are 5 novel genes which appear to associate with androgen sensitivity, which may underlie the strong 4:1 bias towards affected males. Gene expression profiling of 116 LCL from autistic (87) and nonautistic (29) individuals were obtained using a custom-printed DNA microarray containing 39,936 elements (TIGR 40K Human array, GPL3427) and a reference design in which each sample was compared to the Stratagene Universal Human RNA standard. The 87 autistic samples were divided into phenotypic subgroups (language, mild, savant) on the basis of cluster analyses of scores from an autism diagnostic questionnaire, the Autism Diagnostic Interview-Revised instrument. Differentially expressed genes were determined for all autistic vs. control groups, as well as for each of 3 phenotypic ASD groups and controls.
2010-05-17 | E-GEOD-15402 | biostudies-arrayexpress
Project description:Genome-wide DNA methylation profiling of ASD and controls using peripheral blood samples.
2019-09-23 | GSE109905 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below.
2020-09-30 | GSE113701 | GEO
Project description:Autism spectrum disorder (ASD) is a neurodevelopmental disease with complex heterogeneity and aberrations in multiple levels of neurobiology. Recently, our understanding of the molecular abnormalities in ASD has been greatly expanded through transcriptomic analyses of postmortem brains. However, a crucial molecular pathway involved in synaptic development, RNA editing, has not yet been studied on a genome-wide scale. Here we profiled the global patterns of adenosine-to-inosine (A-to-I) editing in a large cohort of ASD cortices and cerebella. Strikingly, we observed a global bias of hypoediting in ASD brains, common to different brain regions and involving many genes with critical neurological function. The large-scale RNA editing changes allowed us to reveal novel insights of RNA editing regulation. Through genome-wide protein-RNA binding analyses and detailed molecular assays, we show that the Fragile X proteins, FMRP and FXR1P, interact with ADAR protens and modulate A-to-I editing. Furthermore, we observed convergent patterns of RNA editing alterations between ASD and Fragile X syndrome, thus establishing RNA editing as a novel molecular link underlying these two highly related diseases. Our findings support a role for RNA editing dysregulation in ASD pathophysiology and highlight novel mechanisms for RNA editing regulation.
2018-12-14 | GSE117776 | GEO
Project description:To examine how activation of different toll-like receptors (TLR) impacts gene expression in Autism Spectrum Disorder (ASD), we cultured peripheral blood monocytes from children with ASD, Pervasive Developmental Disorder Not Otherwise Specified (PDDNOS) or Asperger and typically developing children and treated them with either lipoteichoic acid (LTA) or lipopolysaccharide (LPS) to activate LTR2 or 4 respectively. Following 24 hours of stimulation, we then performed RNA sequencing to profile mRNA responses between non-treated (NT), LTA and LPS treated samples for each diagnosis (control or ASD).
2021-12-17 | GSE140702 | GEO