Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ABSTRACT: Rat model of autism

PROVIDER: PRJNA616070 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR11443149_1.fastq.gz	Fastqsanger.gz
	SRR11443149_2.fastq.gz	Fastqsanger.gz
	SRR11443150_1.fastq.gz	Fastqsanger.gz
	SRR11443150_2.fastq.gz	Fastqsanger.gz
	SRR11443151_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 46

Similar Datasets

Project description:Chinese acupuncture: a potential treatment for autism rat model via improving synaptic function

| PRJNA1131377 | ENA

GNPS_CalTech_murine_model_autism_study_1st_set

Project description:1st dataset for the Caltech autism study in murine model.

2018-01-30 | MSV000082000 | GNPS

GNPS_CalTech_murine_model_autism_study

Project description:2nd dataset for the Caltech autism study in murine model.

2018-01-30 | MSV000081999 | GNPS

Gestational Autoantibody Exposure Alters Early Brain Development in a Rat Model of MAR Autism

Project description:Gestational Autoantibody Exposure Alters Early Brain Development in a Rat Model of MAR Autism

| PRJNA1150899 | ENA

GNPS_CalTech_murine_model_autism_study_2nd_set

Project description:2nd dataset for the Caltech autism study in murine model (updated, full)

2018-01-31 | MSV000082005 | GNPS

Project description:AgxtQ84X rat model

| PRJNA646018 | ENA

Cerebellar oxidative DNA damage and altered DNA methylation in the BTBR T+tf/J mouse model of autism and similarities with human post mortem cerebellum.

Project description:The molecular pathogenesis of autism is complex and involves numerous genomic, epigenomic, proteomic, metabolic, and physiological alterations. Elucidating and understanding the molecular processes underlying the pathogenesis of autism is critical for effective clinical management and prevention of this disorder. The goal of this study is to investigate key molecular alterations postulated to play a role in autism and their role in the pathophysiology of autism. In this study we demonstrate that DNA isolated from the cerebellum of BTBR T+tf/J mice, a relevant mouse model of autism, and from human post-mortem cerebellum of individuals with autism, are both characterized by an increased levels of 8-oxo-7-hydrodeoxyguanosine (8-oxodG), 5-methylcytosine (5mC), and 5-hydroxymethylcytosine (5hmC). The increase in 8-oxodG and 5mC content was associated with a markedly reduced expression of the 8-oxoguanine DNA-glycosylase 1 (Ogg1) and increased expression of de novo DNA methyltransferases 3a and 3b (Dnmt3a and Dnmt3b). Interestingly, a rise in the level of 5hmC occurred without changes in the expression of ten-eleven translocation expression 1 (Tet1) and Tet2 genes, but significantly correlated with the presence of 8-oxodG in DNA. This finding and similar elevation in 8-oxodG in cerebellum of individuals with autism and in the BTBR T+tf/J mouse model warrant future large-scale studies to specifically address the role of genetic alterations in OGG1 in pathogenesis of autism. Gene expression profiles in the cerebellum of 8 weeks old BTBR T+tf/J mice that exhibit an autism-like behavioral phenotype and control C57BL/6J mice were examined using high-throughput Agilent whole genome 8x60K mouse microarrays.

2014-10-23 | E-GEOD-62594 | biostudies-arrayexpress

Gestational Autoantibody Exposure Alters Early Brain Development in a Rat Model of MAR Autism

Project description:Maternal autoantibody related autism (MARA), in which mothers produce specific patterns of autoantibodies during pregnancy, resulting in an autism diagnosis in their offspring, has been observed clinically. Multiple patterns of MARA autoantibodies have been identified clinically, and differences in the severity of the autism phenotype based on the autoantibody pattern have been described. In this study we utilized our preclinical rat model to further elucidate the differential effects of MARA autoantibody exposure based on the known clinical patterns, including the originally identified pattern of lactate dehydrogenase A and B (LDHA/B) + collapsin response mediator protein 1 (CRMP1) + stress-induced phosphoprotein 1 (STIP1) as well as the newly described patterns of CRMP1+CRMP2, CRMP1 + guanine deaminase (GDA), and STIP1+ neuron-specific enolase (NSE). We found that, at postnatal day 2, the levels of brain-specific and serum cytokines/chemokines were altered based on the pattern of MARA autoantibody exposure. Further, we observed changes in the brain transcriptomic profiles that suggest cellular proliferation and differentiation changes due to MARA exposure.

2025-07-02 | GSE275431 | GEO

Amygdala transcriptome in rats prenatally exposed to valproic acid

Project description:The amygdala controls socioemotional behavior and has consistently been implicated in the etiology of Autism Spectrum Disorder (ASD). Precocious amygdala development is commonly reported in ASD youth with the degree of overgrowth positively correlated to the severity of ASD symptoms. However, surprisingly little is known about the cellular, molecular, or genetic changes that occur in the amygdala over development in ASD individuals or rodent models. We examined abnormalities in gene expression in the amygdala and socioemotional behavior across development in the valproic acid (VPA) rat model of ASD.

2017-07-03 | GSE98777 | GEO

Remodeling of synaptic transmission genomic fabrics in the hypothalamic paraventricular nucleus of a rat model of autism

Project description:Remodeling of synaptic transmission genomic fabrics in the hypothalamic paraventricular nucleus of a rat model of autism

| PRJNA526438 | ENA