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Schizo-EPICOG SIGNED

Inflammatory processes underlying cognitive deficits in schizophrenia: epigenetic mechanisms and pharmacological regulation

Total Cost €

0

EC-Contrib. €

0

Partnership

0

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 Schizo-EPICOG project word cloud

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

isolation    neuroinflammmatory    behavioural    psychotic    saha    neuroinflammation    preliminary    epigenetic    inflammatory    gene    traslational    hyperactivity    protein    model    disease    puberty    mechanism    alterations    data    etiopathogenesis    proteins    clozapine    validated    activation    molecular    inmmune    resistant    nuclear    expression    indicate    inhibitor    signalling    relationship    maternal    possibility    modulation    schizophrenic    prenatal    cortex    chronic    markers    event    deacetylases    emerge    acetylation    schizophrenia    clinically    physio    tests    stressful    animal    mouse    subjects    patients    status    excess    prefrontal    mechanisms    followed    effect    psychopathology    hdacs    social    cognitive    involvement    suspected    double    antipsychotics    deficits    prognostic    suggested    matched    vulnerability    controls    priming    phenomenon    histone    regulation    inductor    peripuberty    gestation    drug    treatment    human    induce    minocycline    hdac    neuroinflammatory    free    atypical    hit    worsen    treatments    postmortem    antipsychotic    symptoms   

Project "Schizo-EPICOG" data sheet

The following table provides information about the project.

Coordinator
UNIVERSIDAD DEL PAIS VASCO/ EUSKAL HERRIKO UNIBERTSITATEA 

Organization address
address: BARRIO SARRIENA S N
city: LEIOA
postcode: 48940
website: www.ehu.es

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 Spain [ES]
 Total cost 158˙121 €
 EC max contribution 158˙121 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2016
 Funding Scheme MSCA-IF-EF-ST
 Starting year 2018
 Duration (year-month-day) from 2018-04-11   to  2020-04-10

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    UNIVERSIDAD DEL PAIS VASCO/ EUSKAL HERRIKO UNIBERTSITATEA ES (LEIOA) coordinator 158˙121.00

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 Project objective

'Cognitive deficits represent nuclear symptoms of schizophrenia and are considered prognostic factors of the disease. Moreover, they are resistant to the currently available treatments and it is clinically suspected that atypical antipsychotics might worsen cognitive conditions of schizophrenic patients. Preliminary data indicate the involvement of epigenetic regulation of histone deacetylases (HDACs) in this effect and the possibility of neuroinflammmatory activity as the inductor mechanism. In the etiopathogenesis of schizophrenia a double-hit phenomenon has been suggested. Thus, a prenatal priming event that would induce vulnerability is followed by a second stressful hit in peripuberty. Physio- and psychopathology could emerge from these mechanisms through neuroinflammatory hyperactivity. The aim of the present project is to study the relationship between cognitive deficits and neuroinflammatory activity in a traslational 'double hit' mouse model based on the maternal inmmune activation during gestation followed by social isolation at puberty. In this animal model will be evaluated: 1) Gene and protein expression of inflammatory signalling proteins, HDACs and the status of histone acetylation; 2) Cognitive and psychotic status by means of validated behavioural tests; 3) Modulation of cognitive responses by chronic treatment with the antipsychotic clozapine, the HDAC inhibitor SAHA and the inflammatory activity inhibitor minocycline. Cognitive responses will be related to neuroinflammatory alterations at molecular level. The findings in the animal model will be compared with those obtained in the study of neuroinflammation markers, HDACs expression and histone acetylation status in postmortem human prefrontal cortex of subjects with schizophrenia under antipsychotic treatment or drug-free conditions and matched controls. In these subjects the possibility of an excess of inflammatory activity associated to antipsychotic treatment will be analyzed.'

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