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SCHIZTYPE SIGNED

Brain cell type-specific interactions and schizophrenia

Total Cost €

0

EC-Contrib. €

0

Partnership

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 SCHIZTYPE project word cloud

Explore the words cloud of the SCHIZTYPE project. It provides you a very rough idea of what is the project "SCHIZTYPE" about.

gene    arise    samples    networks    microglia    oligodendrocytes    perturbing    symptomatology    pathological    arrays    personalized    consequence    alterations    molecular    hypothesize    regulatory    genes    neurons    transcription    confirm    cortical    perturbations    epidemiological    genetic    patient    genetically    ultimately    prefrontal    denmark    risk    mouse    independently    pathology    sweden    onset    initiates    functionally    cell    data    cortex    situ    opens    treatment    postmortem    causal    pathologies    clinical    brain    single    fit    relationships    connect    types    transcriptomics    overlapping    material    variously    markers    cellular    brains    tools    excitatory    exploited    heritable    modern    models    light    individual    insights    scz    schizophrenia    expression    unlikely    rna    adulthood    strategies    enriched    putative    multiple    function    expressed    seq    network    model    disease    grns    genomic    underlying    largely    cells    symptoms    containing    mechanisms    lab    inhibitory    tissue   

Project "SCHIZTYPE" data sheet

The following table provides information about the project.

Coordinator
KAROLINSKA INSTITUTET 

Organization address
address: Nobels Vag 5
city: STOCKHOLM
postcode: 17177
website: www.ki.se

contact info
title: n.a.
name: n.a.
surname: n.a.
function: n.a.
email: n.a.
telephone: n.a.
fax: n.a.

 Coordinator Country Sweden [SE]
 Total cost 2˙064˙414 €
 EC max contribution 2˙064˙414 € (100%)
 Programme 1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
 Code Call ERC-2018-COG
 Funding Scheme ERC-COG
 Starting year 2019
 Duration (year-month-day) from 2019-04-01   to  2024-03-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    KAROLINSKA INSTITUTET SE (STOCKHOLM) coordinator 2˙064˙414.00

Map

 Project objective

Schizophrenia is a heritable but genetically complex disease. Pathological and epidemiological data fit a model of SCZ as a network disease with perturbations during brain development leading to early-adulthood onset clinical symptomatology. Our present understanding is based on single markers or arrays of gene expression from tissue samples containing multiple cell types. As a consequence, pathological changes in the function of inhibitory or excitatory neurons, microglia, or oligodendrocytes have variously been proposed to be the cause of symptoms. In light of recent data I hypothesize that it is unlikely that the various cellular SCZ-pathologies all arise independently from genetic alterations in multiple cell types. Recent findings from my lab show that in the cortex the expression of risk genes for SCZ are enriched in excitatory neurons, and that this set of risk-genes is largely non-overlapping with those expressed in other cell types. I propose that pathological genetic changes in excitatory cells ultimately initiates pathological changes in other cell types contributing to the multiple cellular pathologies observed in SCZ. We will: 1. Identify cell type-specific gene regulatory networks involved in SCZ (SCZ-GRNs) in prefrontal cortical excitatory cells by analysis of four distinct SCZ mouse models. 2. Confirm putative SCZ-GRNs in patient material using in situ transcriptomics on postmortem brains and connect to clinical features via collaboration with genomic studies in Sweden and Denmark. 3. Functionally investigate the effects of perturbing excitatory cell SCZ-GRNs on other cell types. Single-cell RNA-seq, providing insights into the molecular properties of individual cells, and modern molecular tools for perturbing transcription in a cell type-specific way opens up for new knowledge of mechanisms underlying SCZ pathology. My work will identify causal relationships that can be exploited for the development of strategies for personalized treatment.

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The information about "SCHIZTYPE" are provided by the European Opendata Portal: CORDIS opendata.

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