Explore the words cloud of the UPR NEURO project. It provides you a very rough idea of what is the project "UPR NEURO" about.
The following table provides information about the project.
THE CHANCELLOR MASTERS AND SCHOLARSOF THE UNIVERSITY OF CAMBRIDGE
|Coordinator Country||United Kingdom [UK]|
|Total cost||1˙979˙286 €|
|EC max contribution||1˙979˙286 € (100%)|
1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
|Duration (year-month-day)||from 2015-09-01 to 2020-08-31|
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|1||THE CHANCELLOR MASTERS AND SCHOLARSOF THE UNIVERSITY OF CAMBRIDGE||UK (CAMBRIDGE)||coordinator||1˙979˙286.00|
This proposal aims to increase our understanding of the role of translational failure in human neurodegenerative diseases. We recently discovered the mechanism by which protein misfolding leads to neurodegeneration in prion disease. The pathway involved is a generic cellular pathway, a branch of the unfolded protein response (UPR) that controls protein synthesis at the level of initiation of translation. Rising levels of misfolded prion protein cause sustained over-activation of the PERK-eIF2α branch of the UPR in neurons resulting in an uncompensated decline in global translation rates, synaptic failure and neuronal death. Reduction of eIF2α-P levels by genetic manipulation or by pharmacological inhibition of PERK, rescue vital translation rates and prevent neurodegeneration and clinical disease in prion-infected mice. There is increasing evidence that UPR dysregulation is a central process in protein misfolding neurodegenerative diseases, and that maintaining translation levels is essential for neuronal health. Raised levels of PERK-P and eIF2α-P occur in brains of patients with Alzheimer’s (AD), Parkinson’s (PD), and related diseases. The pathway is also implicated in learning and memory; manipulation of eIF2α-P levels boost cognition in wild type mice and restore memory deficits in AD mouse models. We will test for over-activation of PERK/eIF2α-P and the effects of its manipulation in other models of neurodegenerative disease. We will generate new transgenic mouse models that isolate translational failure from specific misfolded proteins and use these to gain valuable new insights into the window for intervention when neurons can still be rescued, the selective vulnerability of different neuronal populations, and the role of the UPR in neurons and glia. Collectively, the aim is to increase insight into the role of UPR-mediated translational failure in human neurodegenerative disease and determine its tractability for the treatment of dementia.
|year||authors and title||journal||last update|
Helois Radford, Julie A. Moreno, Nicholas Verity, Mark Halliday, Giovanna R. Mallucci
PERK inhibition prevents tau-mediated neurodegeneration in a mouse model of frontotemporal dementia
published pages: 633-642, ISSN: 0001-6322, DOI: 10.1007/s00401-015-1487-z
|Acta Neuropathologica 130/5||2020-01-17|
Heather L. Smith, Giovanna R. Mallucci
The unfolded protein response: mechanisms and therapy of neurodegeneration
published pages: 2113-2121, ISSN: 0006-8950, DOI: 10.1093/brain/aww101
Sophie J. Bradley, Julie-Myrtille Bourgognon, Helen E. Sanger, Nicholas Verity, Adrian J. Mogg, David J. White, Adrian J. Butcher, Julie A. Moreno, Colin Molloy, Timothy Macedo-Hatch, Jennifer M. Edwards, Jurgen Wess, Robert Pawlak, David J. Read, Patrick M. Sexton, Lisa M. Broad, Joern R. Steinert, Giovanna R. Mallucci, Arthur Christopoulos, Christian C. Felder, Andrew B. Tobin
M1 muscarinic allosteric modulators slow prion neurodegeneration and restore memory loss
published pages: 487-499, ISSN: 0021-9738, DOI: 10.1172/JCI87526
|Journal of Clinical Investigation 127/2||2020-01-17|
Lisa Michelle Restelli, BjÃ¶rn Oettinghaus, Mark Halliday, Cavit Agca, Maria Licci, Lara Sironi, Claudia Savoia, JÃ¼rgen Hench, Markus Tolnay, Albert Neutzner, Alexander Schmidt, Anne Eckert, Giovanna Mallucci, Luca Scorrano, Stephan Frank
Neuronal Mitochondrial Dysfunction Activates the Integrated Stress Response to Induce Fibroblast Growth Factor 21
published pages: 1407-1414, ISSN: 2211-1247, DOI: 10.1016/j.celrep.2018.07.023
|Cell Reports 24/6||2020-01-17|
Mark Halliday, Daniel Hughes, Giovanna R. Mallucci
Fine-tuning PERK signaling for neuroprotection
published pages: 812-826, ISSN: 0022-3042, DOI: 10.1111/jnc.14112
|Journal of Neurochemistry 142/6||2020-01-17|
Oliver J. Freeman, Giovanna R. Mallucci
The UPR and synaptic dysfunction in neurodegeneration
published pages: 530-537, ISSN: 0006-8993, DOI: 10.1016/j.brainres.2016.03.029
|Brain Research 1648||2020-01-17|
Mark Halliday, Helois Radford, Karlijn A. M. Zents, Collin Molloy, Julie A. Moreno, Nicholas C. Verity, Ewan Smith, Catharine A. Ortori, David A. Barrett, Martin Bushell, Giovanna R. Mallucci
Repurposed drugs targeting eIF2Î±-P-mediated translational repression prevent neurodegeneration in mice
published pages: 1768-1783, ISSN: 0006-8950, DOI: 10.1093/brain/awx074
I Celardo, A C Costa, S Lehmann, C Jones, N Wood, N E Mencacci, G R Mallucci, S H Y Loh, L M Martins
Mitofusin-mediated ER stress triggers neurodegeneration in pink1/parkin models of Parkinsonâ€™s disease
published pages: e2271, ISSN: 2041-4889, DOI: 10.1038/cddis.2016.173
|Cell Death and Disease 7/6||2020-01-17|
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