DRASTIC

"Apathy in schizophrenia: time for a DRASTIC (Dual Routes to Apathy in Schizophrenia: Treatment, Imaging, Cognition) study"

 Coordinatore ACADEMISCH ZIEKENHUIS GRONINGEN 

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 Nazionalità Coordinatore Netherlands [NL]
 Totale costo 1˙499˙780 €
 EC contributo 1˙499˙780 €
 Programma FP7-IDEAS-ERC
Specific programme: "Ideas" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013)
 Code Call ERC-2012-StG_20111124
 Funding Scheme ERC-SG
 Anno di inizio 2013
 Periodo (anno-mese-giorno) 2013-04-01   -   2018-03-31

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    ACADEMISCH ZIEKENHUIS GRONINGEN

 Organization address address: Hanzeplein 1
city: GRONINGEN
postcode: 9713 GZ

contact info
Titolo: Ms.
Nome: Johanna M
Cognome: Van Apeldoorn
Email: send email
Telefono: +31 50 3633040
Fax: +31 50 3632883

NL (GRONINGEN) hostInstitution 1˙499˙780.00
2    ACADEMISCH ZIEKENHUIS GRONINGEN

 Organization address address: Hanzeplein 1
city: GRONINGEN
postcode: 9713 GZ

contact info
Titolo: Prof.
Nome: Andreas
Cognome: Aleman
Email: send email
Telefono: 31503635111
Fax: 31503638575

NL (GRONINGEN) hostInstitution 1˙499˙780.00

Mappa


 Word cloud

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first    hypothesis    frontostriatal    cognitive    cortex    primarily    sea    ca    right    apathy    forms    neural    basis    patients    emotional    treatment    circuit   

 Obiettivo del progetto (Objective)

'Apathy is a prominent and severely debilitating aspect of several psychiatric disorders, most notably schizophrenia. Little is known regarding the neuroscientific basis of apathy, however. Clinically, it has been suggested that two forms of apathy can be distinguished: cognitive apathy (CA) which concerns reduced initiative to start daily activities and social-emotional apathy (SEA) which concerns reduced interest in otherwise gratifying activities. I hypothesize that CA is primarily a dysfunction of cognitive control and self-initiated action, whereas SEA is primarily a failure to signal the salience of positive events. The present project, for the first time, tests the hypothesis that two neuroanatomically distinct routes underlie these two forms of apathy: a dorsal frontostriatal circuit including also the right parietal cortex for CA (associated with abnormalities of glutamate neurotransmission), and a more ventral frontostriatal circuit including the reward system for SEA (involving abnormal dopamine transmission). The objective of this project is threefold. First, to investigate the two neural circuits in relation to the two forms of apathy using functional MRI and positron emission tomography. Second, I will test the hypothesis that CA is associated with poorer long-term functioning using longitudinal data. Third, we will conduct a controlled treatment study of a novel intervention to improve CA: transcranial magnetic stimulation over the right prefrontal cortex to target the relevant network. Thus, the present proposal aims to elucidate fundamental cognitive and emotional processes underlying apathy by unravelling the neural basis of two pathways that may lead to apathy. Last but not least, the treatment study may contribute to novel strategies that will ultimately improve patients’ lives. The results will also have implications for understanding apathy in patients with depression, brain damage and neurodegenerative diseases.'

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