Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

MicroRNA therapeutics for stratified treatment of Schizophrenia

ABSTRACT: MicroRNA therapeutics for stratified treatment of Schizophrenia

PROVIDER: PRJNA929968 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR23289807.fastq.gz	Fastqsanger.gz
	SRR23289808.fastq.gz	Fastqsanger.gz
	SRR23289809.fastq.gz	Fastqsanger.gz
	SRR23289810.fastq.gz	Fastqsanger.gz
	SRR23289811.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 29

Similar Datasets

MicroRNA therapeutics for stratified treatment of Schizophrenia

Project description:Schizophrenia (SZ) is a devastating psychiatric illness affecting 1% of the world population. In addition to genetic predisposition, environmental factors contribute to the risk for developing SZ. Such genome environment interactions frequently activate epigenetic and epitranscriptomic mechansims. There are emerging evidence that genetic and environmental risk factors merge at the level of microRNA expression, which are discussed as biomarker and therapeutic target in various disorders including neuropsychiatric diseases. In this study we analyzed the blood microRNAome of healthy individuals and SZ patients via small RNA sequencing. By combining these data with a corresponding analysis of post-mortem human brain tissue, we identify one candidate microRNA that is down-regulated in patients. Moreover, its expression is significantly correlated to disease phenotypes. Manipulation of this microRNAs in mouse prefrontal cortex causes schizophrenia-like phenotypes. Functional analysis revealed the cellular processes affected by this microRNA and allowed us to develop an arsenal of RNA-based therapeutic approaches that are able to ameliorate molecular disease phenotypes in mouse and human-based cellular systems as well as the behavioral phenotypes. In conclusion, we identify a novel microRNA as target for stratified RNA-therapeutics in schizophrenia.

2024-03-26 | GSE224142 | GEO

MiRNA Differences Related to Treatment Resistant Schizophrenia

Project description:Schizophrenia (SZ) is a serious mental disorder that is typically treated with antipsychotic medication. Treatment-resistant schizophrenia (TRS) is the condition where symptoms remain after pharmacological intervention, resulting in long-lasting functional and social impairments. As the identification and treatment of a TRS patient requires previous failed treatments, early mechanisms of detection are needed in order to quicken the access to effective therapy, as well as improve treatment adherence. In this study, we aim to find a microRNA (miRNA) signature for TRS, as well as to shed some light on the molecular pathways potentially involved in this severe condition. To do this, we compared the blood miRNAs of schizophrenia patients that respond to medication and TRS patients, thus obtaining a 16-miRNA TRS profile. Then, we assessed the ability of this signature to separate responders and TRS patients using hierarchical clustering, observing that most of them are grouped correctly (~70% accuracy). We also conducted a network, pathway analysis, and bibliography search to spot molecular pathways potentially altered in TRS. We found that the response to stress seems to be a key factor in TRS and that proteins p53, SIRT1, MDM2, and TRIM28 could be the potential mediators of such responses. Finally, we suggest a molecular pathway potentially regulated by the miRNAs of the TRS profile.

2023-01-18 | GSE223043 | GEO

Aripiprazol treatment on schizophrenia patients

Project description:Transcriptional effects of Aripiprazol treatment on schizophrenia patients.

| PRJEB42627 | ENA

MiRNA Differences Related to Treatment Resistant Schizophrenia

Project description:MiRNA Differences Related to Treatment Resistant Schizophrenia

| PRJNA924754 | ENA

Genome-wide microRNA transcriptome profiles in Control and Schizophrenia hiPSC-dervied NPC [miRNA-seq]

Project description:We Report the genome-wide RNA expression levels in control and schizophrenia hiPSC dervied NPC treated with neuronal media for 2 days. In total, 440 microRNA expression were detected in all samples, of which 16 were dysregualted.

2017-06-01 | GSE92875 | GEO

Blood methylomes of schizophrenia patients differing in their response to risperidone treatment

Project description:Schizophrenia patients vary in their response to antipsychotic (AP) treatment and predicting if and which therapy will be efficient is of high clinical and social importance. Here, we set out to analyze blood methylomes of 28 schizophrenia patients just before starting (baseline) risperidone treatment and four weeks later (follow-up) in order to look for differences that may help predict variation in response. We were not able to identify CpGs whose baseline methylation could be used as a predictive biomarker, but our analysis suggests the role of methylation status of genes involved in immunity, neurotransmission and neuronal development in the treatment response.

2023-03-19 | E-MTAB-11921 | biostudies-arrayexpress

Schizophrenia-related microdeletion causes progressive brain ventricle enlargement through microRNA-dependent deceleration of motile cilia beating

Project description:Progressive ventricular enlargement is one of the most reproducible and recognizable structural abnormalities in schizophrenia, and is associated with more severe symptoms and poorer clinical outcome. The mechanisms of ventricular enlargement in schizophrenia is unknown. We identified that progressive ventricular enlargement is associated with deceleration of motile cilia beating in ependymal cells lining ventricular walls in murine models of schizophrenia-associated 22q11 deletion syndrome (22q11DS). The cilia beating deficit is caused by an aberrant elevation of Drd1, which is highly enriched in the motile cilia. Haploinsufficiency of the microRNA-processing gene Dgcr8 is responsible for the Drd1 elevation in ependymal cells of 22q11DS mice, and is mediated by reduction of Drd1-targeting microRNAs miR-674-3p and miR-382-3p. Replenishing miR-674-3p or miR-382-3p in 22q11DS mice rescued the motile cilia beating abnormalities and normalized the ventricular size. Knockdown of these microRNA mimicked cilia beating and ventricular deficits. Ventricular enlargement was also caused by Crispr/cas9-mediated deletion of the Drd1 seed site for miR-674-3p/miR-382-3p. This suggests that Dgcr8-miR-674-3p/miR-382-3p-Drd1–dependent disruption of cilia motility in ependymal cells is a pathogenic event underlying schizophrenia-associated ventricular enlargement.

2019-12-07 | GSE123560 | GEO

New host-directed therapeutics for the treatment of Clostridioides difficile infection

Project description:New host-directed therapeutics for the treatment of Clostridioides difficile infection

| PRJNA603301 | ENA

Schizophrenia metagenome

Project description:Schizophrenia metagenome

| PRJEB29415 | ENA

Transcription profiling of rat brain after treatment with narcoleptics used in the treatment of human schizophrenia

Project description:In pevious research we have shown that the disruption of the normal development of the ventral hippocampus in rodents leads to cellular abnormalities in the frontal cortex and behavioral deficits related to schizophenia (Neurotox Res. 2002, 4(5-6):469-475). We propose the use of gene expression analysis to investigate the molecular underpinnings of these processes which may shed light on the molecular processes relevant to human schizophrenia. In addition, we seek to characterize expression differences induced by chronic administration of antipsychotic medications, which may give insight into the molecular processes involved in ameliorating psychotic symptoms. Using both surgical and drug interventions, we aim to examine experimentally induced expression differences in the rodent brain that are relevant to human neuropsychiatric disorders. Disruption of the normal development of the vental hippocampus or chronic neuroleptic administration, will result in gene expression changes in the frontal cortex of rats. Elucidation of the molecular cascades underlying these treatments will shed light on both the pathoetiology (from the lesion experiments) and theurapeutic processes (from the antipsychotic treatment experiments) involved in human schizophrenia. We have developed 3 groups of samples:; 1] Ventral hippocampal lesion in neonatal rats (treatment and controls, total N=22); 2] Tetrodotoxin disruption of the ventral hippocampus (treatment and controls, total N=20); 3] Chronic administration of neuroleptics (multiple drugs, multiple doses, and controls, total N=63) Grand Total N=105

2008-06-12 | E-GEOD-4031 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data