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INTEGRATE SIGNED

An integrated hypothesis for cognitive and positive symptoms in schizophrenia

Total Cost €

EC-Contrib. €

Partnership

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INTEGRATE project word cloud

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

withdrawal neurons hyperdopaminergia symptoms mechanisms unbalance excitation probably pathophysiological hypothesis negative social delusions psychosis treating an restore antipsychotics underlie cognitive hallucinations disorder mice seem prevent brain arise treatment schizophrenia ineffective developmental clusters consisted motivation dopaminergic suggest dysfunctional midbrain function assumed memory abnormal receptors inhibition last positive dopamine largely frequently striatal model normalizing executive deficits cortical verified mostly

Project "INTEGRATE" data sheet

The following table provides information about the project.

Coordinator	UNIVERSITETET I OSLO Organization address address: PROBLEMVEIEN 5-7 city: OSLO postcode: 313 website: www.uio.no 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	Norway [NO]
Total cost	208˙400 €
EC max contribution	208˙400 € (100%)
Programme	1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
Code Call	H2020-MSCA-IF-2017
Funding Scheme	MSCA-IF-EF-ST
Starting year	2018
Duration (year-month-day)	from 2018-12-01 to 2021-12-01

Partnership

Take a look of project's partnership.

#	participants	country	role	EC contrib. [€]
1	UNIVERSITETET I OSLO UNIVERSITETET I OSLO Organization address address: PROBLEMVEIEN 5-7 city: OSLO postcode: 313 website: www.uio.no contact info title: n.a. name: n.a. surname: n.a. function: n.a. email: n.a. telephone: n.a. fax: n.a.	NO (OSLO)	coordinator	208˙400.00

Map

Project objective

An integrated hypothesis for cognitive and positive symptoms in schizophrenia:

Schizophrenia is a complex developmental brain disorder with three main clusters of symptoms: (i) positive (psychosis, delusions and hallucinations), (ii) negative (reduced motivation and social withdrawal), and (iii) cognitive (memory and executive function deficits). For the last 50 years, the only effective treatment has consisted of antipsychotics targeting dopamine receptors. Yet, antipsychotics control mostly the positive symptoms and are largely ineffective at treating other deficits.

It is frequently assumed that distinct pathophysiological mechanisms underlie different symptoms. Psychosis is associated with striatal hyperdopaminergia, probably due to abnormal activity of midbrain dopaminergic neurons. Yet cognitive deficits seem to arise from cortical excitation/inhibition unbalance. I propose to test, in a mice model, the hypothesis that striatal hyperdopaminergia results from dysfunctional cortical inhibition. If verified, this would suggest that normalizing cortical activity in schizophrenia might both restore cognitive function and prevent psychosis.

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