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A gene co-expression network in whole blood of schizophrenia patients is independent of antipsychotic-use and enriched for brain-expressed genes

ABSTRACT: A gene co-expression network in whole blood of schizophrenia patients is independent of antipsychotic-use and enriched for brain-expressed genes

PROVIDER: PRJNA168016 | ENA |

REPOSITORIES: ENA

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A gene co-expression network in whole blood of schizophrenia patients is independent of antipsychotic-use and enriched for brain-expressed genes

Project description:This SuperSeries is composed of the following subset Series: GSE38481: A gene co-expression network in whole blood of schizophrenia patients is independent of antipsychotic-use and enriched for brain-expressed genes [HumanRef-8 v3.0] GSE38484: A gene co-expression network in whole blood of schizophrenia patients is independent of antipsychotic-use and enriched for brain-expressed genes [HumanHT-12 V3.0] Refer to individual Series

2012-07-08 | E-GEOD-38485 | biostudies-arrayexpress

A gene co-expression network in whole blood of schizophrenia patients is independent of antipsychotic-use and enriched for brain-expressed genes [HumanRef-8 v3.0]

Project description:Gene expression analyses in whole blood reveal a network of genes related to schizophrenia Weighted gene co-expression analyses applied to human whole blood gene expression data of schizophrenia cases and healthy controls

2012-07-08 | E-GEOD-38481 | biostudies-arrayexpress

A gene co-expression network in whole blood of schizophrenia patients is independent of antipsychotic-use and enriched for brain-expressed genes [HumanHT-12 V3.0]

2012-07-08 | E-GEOD-38484 | biostudies-arrayexpress

A gene co-expression network in whole blood of schizophrenia patients is independent of antipsychotic-use and enriched for brain-expressed genes [HumanRef-8 v3.0]

Project description:Gene expression analyses in whole blood reveal a network of genes related to schizophrenia

2012-07-09 | GSE38481 | GEO

A gene co-expression network in whole blood of schizophrenia patients is independent of antipsychotic-use and enriched for brain-expressed genes [HumanHT-12 V3.0]

Project description:Gene expression analyses in whole blood reveal a network of genes related to schizophrenia

2012-07-09 | GSE38484 | GEO

Transcription profiling of brain samples from human control and schizophrenia patients who were treated with either typical, atypical or no antipsychotic medication

Project description:Multiple studies have shown that brain gene expression is disturbed in subjects suffering from schizophrenia. However, disentangling disease effects from alterations caused by neuroleptics is a challenging task. <br> To address the issues of disease heterogeneity and the effect of antipsychotic medication, we use a large collection of 110 brain autopsy samples, subdivided according to the type of antipsychotic medication received. We use global and high-resolution mRNA quantification techniques to analyse gene expression in brain tissues. We also analyse transcription in-vitro, in cell lines before and after treatment with cytokines.<br> Results. We show that inflammation-related genes are up regulated in all groups of patients, including those not treated at the time of death. In particular, four co-expressed genes that are inducible by inflammatory cytokines showed increased mRNA levels, namely IFITM2, IFITM3, SERPINA3, and GBP1 (p-values from qPCR ? 0.01). We also show that these genes are expressed in oligodendrocyte and endothelial cell lines, and transcription is inducible by inflammatory cytokines in both cell lines. Our results give molecular support to the inflammatory theory of schizophrenia and suggest that inflammatory cytokines may stimulate transcription in endothelial brain cells during schizophrenia progression. Unexpectedly, inflammation-related genes may also have a role in myelin producing cells, since they are also inducible by cytokines in oligodendrocyte cell lines. Our findings encourage future research to explore whether anti-inflammatory agents can be used in combination with traditional antipsychotics for a more efficient treatment of schizophrenia.

2007-12-06 | E-MEXP-857 | biostudies-arrayexpress

Assess the effects of antipsychotic use on gene expression changes in dementia

Project description:In order to elucidate mechanisms underlying adverse effects of antipsychotic use in dementia we generated gene expression signatures for three antipsychotics representing a range of mechanisms of action relevant to the current landscape of drug development and clinical use in dementia: amisulpride (primarily a D2/D3 antagonist), risperidone (primarily a 5HT2A/D2 antagonist) and volinanserin (highly selective 5HT2A inverse agonist). We reported that the antipsychotic signatures would be score positively with conditions and diseases related to known side effects of their use in dementia such as cardiovascular and infectious diseases.

2020-04-30 | GSE149611 | GEO

Hippocampal Subfield Transcriptome Analysis in Schizophrenia Psychosis

Project description:We have previously demonstrated functional and molecular changes in hippocampal subfields in individuals with schizophrenia (SZ) psychosis associated with hippocampal excitability. In this study, we use RNA-seq and assess global transcriptome changes in the hippocampal subfields, DG, CA3, and CA1 from individuals with SZ psychosis and controls to elucidate subfield-relevant molecular changes. We also examine changes in gene expression due to antipsychotic medication in the hippocampal subfields from our SZ ON- and OFF-antipsychotic medication cohort. We identify unique subfield-specific molecular profiles in schizophrenia postmortem samples compared to controls, implicating astrocytes in DG, immune mechanisms in CA3, and synaptic scaling in CA1. We show a unique pattern of subfield-specific effects by antipsychotic medication on gene expression levels with scant overlap of genes differentially expressed by SZ disease effect versus medication effect. These hippocampal subfield changes could provide the basis for previously observed hippocampal SZ pathology and explain the lack of full efficacy of conventional antipsychotic medication on SZ symptomatology. With further characterization, the identified distinct molecular profiles of the DG, CA3, and CA1 in SZ psychosis may serve to identify potential hippocampal-based therapeutic targets.

2020-05-11 | GSE138082 | GEO

A gene co-expression network in whole blood of schizophrenia patients is independent of antipsychotic-use and enriched for brain-expressed genes

Project description:This SuperSeries is composed of the SubSeries listed below.

2012-07-09 | GSE38485 | GEO

Gene expression changes following chronic antipsychotic exposure in single cells from mouse striatum

Project description:Background. Schizophrenia is an idiopathic psychiatric disorder with a high degree of polygenicity. Evidence from genetics, single-cell, and pharmacological studies suggest an important overlap between genes involved in the etiology of schizophrenia and the cellular mechanisms of action of antipsychotics in medium spiny neurons (MSNs). Methods. We applied single-cell RNA-sequencing to striatal samples from C57BL/6J mice chronically exposed to a typical antipsychotic (haloperidol), an atypical antipsychotic (olanzapine), or placebo. We implemented careful statistical analyses to identify differentially expressed genes in two cell populations identified from the single-cell RNA-sequencing (MSNs and microglia) and applied multiple analysis pipelines to contextualize these findings. Results. Differential expression analysis showed that there was a larger share of differentially expressed genes (DEGs) in MSNs from mice treated with olanzapine vs. haloperidol. DEGs were enriched in broad loci implicated by genetic studies of schizophrenia, and we highlighted nine genes with convergent evidence. Pathway analyses highlighted alternative splicing, mitochondrial function, and neuron and synapse development as particularly engaged by antipsychotics. In microglia, we identified pathways involved in microglial activation and inflammation as part of the antipsychotic response. Conclusions. Our goal was to evaluate connections between schizophrenia genetic findings and cellular gene expression changes following antipsychotic exposure. We found that differential gene expression in MSNs from mice chronically treated with olanzapine converges on similar pathways and gene sets.

2021-04-14 | GSE171977 | GEO

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