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EU funding (€8,838,000): Inflammation and AD: modulating microglia function focussing on TREM2 and CD33 - Sofia ref.: 115976 Hor1 Nov 2016 EU Research and Innovation programme "Horizon"
Overview
Text
Inflammation and AD: modulating microglia function focussing on TREM2 and CD33 - Sofia ref.: 115976
Alzheimer’s disease (AD) is an age-related chronic neurodegenerative disease with four main pathological changes in the brain: amyloid plaques, fibrillary tau tangles, inflammation and neuronal loss. Phagocytes around amyloid plaques in late onset AD (LOAD) may be neurotoxic but have limited motility and phagocytic activity, suggesting a dysfunctional activation. These phagocytes express the innate immune receptor TREM2 and CD33. Variants of both genes have been linked to LOAD. The main objectives of PHAGO are to find means of modulating microglia/macrophage activation via TREM2, CD33 and related signalling pathways, and determine the effects of such modulation on microglia/macrophage function, amyloid-β and neurodegeneration, in order to find a treatment for AD. PHAGO will deliver well characterized tools and knowledge through which to manipulate AD risk and provide targets and markers ready to progress to drug development. PHAGO will realise this goal by comprehensively attacking the problem simultaneously at multiple levels, including the molecular structures of the receptors, receptor ligand interactions, ectodomain function in vitro and in vivo, characterisation of receptor processing, modification and signalling, receptor-regulated signalling pathways, gene expression and phagocyte function in cells and animals, comprehensive analysis of receptor knock-in and knock-out models crossed to two different animal models of AD, and identification of receptor-related biomarkers in AD patients. Innovative approaches of PHAGO will include identification of new AD-risk genes using a TREM2 co-expression network approach, brain imaging of AD patients with TREM2 and CD33 variants, and generation of patient iPSC-derived microglia/macrophages to comprehensively phenotype gene variants. The project will also generate tools, such as ligands, reporter cells and optimised assays, suitable for further development of treatments targeting TREM2 and/or CD33 in AD.
Funded Companies:
| Company name | Funding amount |
| ABBVIE DEUTSCHLAND GmbH & Co. KG | €0.00 |
| ARTTIC INNOVATION GmbH | €0.00 |
| Arttic | €593,750 |
| Astrazeneca AB | €0.00 |
| Axxam S.p.A. | €438,750 |
| CHARITE - UNIVERSITAETSMEDIZIN BERLIN | €538,750 |
| DEUTSCHES ZENTRUM für NEURODEGENERATIVE ERKRANKUNGEN e. V. | €1,027,500 |
| Eisai Ltd. | €0.00 |
| Eli Lilly and Company Ltd. | €0.00 |
| F. HOFFMANN-LA ROCHE AG | €0.00 |
| FRAUNHOFER GESELLSCHAFT ZUR FORDERUNG DER ANGEWANDTEN FORSCHUNG e. V. | €500,000 |
| Goeteborgs Universitet | €372,156 |
| H. Lundbeck AS | €0.00 |
| Janssen Pharmaceutica N.V. | €0.00 |
| King's College London | €1,115,000 |
| LIFE AND BRAIN GmbH | €451,250 |
| ORION Oyj | €0.00 |
| Sanofi-Aventis Recherche & Developpement | €0.00 |
| The Chancellor Masters and Scholars of the University of Cambridge | €1,052,500 |
| €1,754,200 | |
| €994,144 |
Source: https://cordis.europa.eu/project/id/115976
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