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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

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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.

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

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

Map

 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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