Opendata, web and dolomites
  1. home
  2. trasparenza
  3. open h2020
  4. schizo-epicog

Schizo-EPICOG SIGNED

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

Total Cost €

0

EC-Contrib. €

0

Partnership

0

Views

0

 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.

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

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.'

Are you the coordinator (or a participant) of this project? Plaese send me more information about the "SCHIZO-EPICOG" project.

For instance: the website url (it has not provided by EU-opendata yet), the logo, a more detailed description of the project (in plain text as a rtf file or a word file), some pictures (as picture files, not embedded into any word file), twitter account, linkedin page, etc.

Send me an  email (fabio@fabiodisconzi.com) and I put them in your project's page as son as possible.

Thanks. And then put a link of this page into your project's website.

The information about "SCHIZO-EPICOG" are provided by the European Opendata Portal: CORDIS opendata.

More projects from the same programme (H2020-EU.1.3.2.)

LiverMacRegenCircuit (2020)

Elucidating the role of macrophages in liver regeneration and tissue unit formation

Read More  

MY MITOCOMPLEX (2021)

Functional relevance of mitochondrial supercomplex assembly in myeloid cells

Read More  

CODer (2020)

The molecular basis and genetic control of local gene co-expression and its impact in human disease

Read More