GLORIA

Understanding chronic pain and new druggable targets: Focus on glial-opioid receptor interface

 Coordinatore HELSINGIN YLIOPISTO 

 Organization address address: YLIOPISTONKATU 4
city: HELSINGIN YLIOPISTO
postcode: 14

contact info
Titolo: Mrs.
Nome: Tiina
Cognome: Berg
Email: send email
Telefono: +358 919125129

 Nazionalità Coordinatore Finland [FI]
 Totale costo 7˙825˙178 €
 EC contributo 5˙997˙079 €
 Programma FP7-HEALTH
Specific Programme "Cooperation": Health
 Code Call FP7-HEALTH-2013-INNOVATION-1
 Funding Scheme CP-FP
 Anno di inizio 2013
 Periodo (anno-mese-giorno) 2013-11-01   -   2018-10-31

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    HELSINGIN YLIOPISTO

 Organization address address: YLIOPISTONKATU 4
city: HELSINGIN YLIOPISTO
postcode: 14

contact info
Titolo: Mrs.
Nome: Tiina
Cognome: Berg
Email: send email
Telefono: +358 919125129

FI (HELSINGIN YLIOPISTO) coordinator 2˙118˙688.50
2    KAROLINSKA INSTITUTET

 Organization address address: Nobels Vag 5
city: STOCKHOLM
postcode: 17177

contact info
Titolo: Mrs.
Nome: Ylva
Cognome: Hultman
Email: send email
Telefono: +46 8 524 832 44

SE (STOCKHOLM) participant 2˙011˙123.20
3    CENTRE EUROPEEN DE RECHERCHE EN BIOLOGIE ET MEDECINE

 Organization address address: Rue Laurent Fries 1
city: ILLKIRCH GRAFFENSTADEN
postcode: 67404

contact info
Titolo: Dr.
Nome: Steve
Cognome: Brooks
Email: send email
Telefono: +3 33 88 65 33 94

FR (ILLKIRCH GRAFFENSTADEN) participant 974˙800.00
4    JOHANN WOLFGANG GOETHE UNIVERSITAET FRANKFURT AM MAIN

 Organization address address: GRUNEBURGPLATZ 1
city: FRANKFURT AM MAIN
postcode: 60323

contact info
Titolo: Prof.
Nome: Jörn
Cognome: Lötsch
Email: send email
Telefono: +49 69 6301 4589
Fax: +49 69 6301 7636

DE (FRANKFURT AM MAIN) participant 578˙396.80
5    CHEMEDEST OU

 Organization address address: SOOLA 8
city: TARTU
postcode: 51013

contact info
Titolo: Mr.
Nome: Leonid
Cognome: Tolstov
Email: send email
Telefono: +372 5049961

EE (TARTU) participant 314˙070.60

Mappa


 Word cloud

Esplora la "nuvola delle parole (Word Cloud) per avere un'idea di massima del progetto.

models    validated    experimental    animal    analgesics    patients    drug    activation    pain    profile    differences    studied    opioids    tests    inflammatory    neuropathic    glial    compounds    arthritis    biomarker    fibromyalgia    perception    chronic   

 Obiettivo del progetto (Objective)

'Chronic pain is prevalent and it causes decreased quality of life and significant costs to the society in terms of lost working capacity. Currently available analgesics are either not effective enough or patients cannot take them due to adverse effects. Non-steroidal anti-inflammatory drugs are a major cause of drug-related morbidity and mortality. Opioids can cause tolerance and addiction when used for long-term management of chronic pain. Analgesic efficacy can be improved by targeting specific mechanisms that are involved in pain processing of specific conditions, e.g. fibromyalgia, osteoarthritis, rheumatoid arthritis, and neuropathic pain, and by improving the safety profile of the current analgesics. This project focuses on the role of glial activation by tissue and nerve injury, inflammation, and opioids in large cohorts of chronic pain patients. We will develop a biomarker profile for the clinical conditions by assessing inflammatory markers in cerebrospinal fluid and glial activation in the brain with PET, by performing well-validated experimental pain tests, and genetics. Interindividual differences in pain perception will be studied using experimental pain tests including activation of descending inhibitions as a biomarker of endogenous analgesia and fMRI. Individual differences with the glial activation and pain perception will be used to design different research lines across the board aiming at developing personalized treatments for pain. We will use well-validated animal models relevant for arthritis, fibromyalgia, and neuropathic pain. Glial activation in these animal models will be studied using novel methodology to better understand the pathophysiology of these conditions. They will also be used as targets for new drug discovery which will focus on the design and synthesis of compounds that block TLR4-mediated activation of glia and also on small compounds that mimic the actions of the GDNF-family.'

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