Explore the words cloud of the ALZSYN project. It provides you a very rough idea of what is the project "ALZSYN" about.
The following table provides information about the project.
THE UNIVERSITY OF EDINBURGH
|Coordinator Country||United Kingdom [UK]|
|Total cost||2˙000˙000 €|
|EC max contribution||2˙000˙000 € (100%)|
1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
|Duration (year-month-day)||from 2016-11-01 to 2021-10-31|
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|1||THE UNIVERSITY OF EDINBURGH||UK (EDINBURGH)||coordinator||2˙000˙000.00|
Alzheimer's disease, the most common cause of dementia in older people, is a devastating condition that is becoming a public health crisis as our population ages. Despite great progress recently in Alzheimer’s disease research, we have no disease modifying drugs and a decade with a 99.6% failure rate of clinical trials attempting to treat the disease. This project aims to develop relevant therapeutic targets to restore brain function in Alzheimer’s disease by integrating human and model studies of synapses. It is widely accepted in the field that alterations in amyloid beta initiate the disease process. However the cascade leading from changes in amyloid to widespread tau pathology and neurodegeneration remain unclear. Synapse loss is the strongest pathological correlate of dementia in Alzheimer’s, and mounting evidence suggests that synapse degeneration plays a key role in causing cognitive decline. Here I propose to test the hypothesis that the amyloid cascade begins at the synapse leading to tau pathology, synapse dysfunction and loss, and ultimately neural circuit collapse causing cognitive impairment. The team will use cutting-edge multiphoton and array tomography imaging techniques to test mechanisms downstream of amyloid beta at synapses, and determine whether intervening in the cascade allows recovery of synapse structure and function. Importantly, I will combine studies in robust models of familial Alzheimer’s disease with studies in postmortem human brain to confirm relevance of our mechanistic studies to human disease. Finally, human stem cell derived neurons will be used to test mechanisms and potential therapeutics in neurons expressing the human proteome. Together, these experiments are ground-breaking since they have the potential to further our understanding of how synapses are lost in Alzheimer’s disease and to identify targets for effective therapeutic intervention, which is a critical unmet need in today’s health care system.
|year||authors and title||journal||last update|
Marta Querol-Vilaseca, MartÃ Colom-Cadena, Jordi Pegueroles, RaÃºl NuÃ±ez-Llaves, Joan Luque-Cabecerans, Laia MuÃ±oz-Llahuna, Jordi Andilla, Olivia Belbin, Tara L. Spires-Jones, Ellen Gelpi, Jordi Clarimon, Pablo Loza-Alvarez, Juan Fortea, Alberto LleÃ³
Nanoscale structure of amyloid-Î² plaques in Alzheimerâ€™s disease
published pages: , ISSN: 2045-2322, DOI: 10.1038/s41598-019-41443-3
|Scientific Reports 9/1||2020-01-24|
Eleanor K. Pickett, Christopher M. Henstridge, Elizabeth Allison, Rose Pitstick, Amy Pooler, Susanne Wegmann, George Carlson, Bradley T. Hyman, Tara L. Spires-Jones
Spread of tau down neural circuits precedes synapse and neuronal loss in the rTgTauEC mouse model of early Alzheimer\'s disease
published pages: e21965, ISSN: 0887-4476, DOI: 10.1002/syn.21965
Rosemary J Jackson, Jamie Rose, Jane Tulloch, Chris Henstridge, Colin Smith, Tara L Spires-Jones
Clusterin accumulates in synapses in Alzheimerâ€™s disease and is increased in apolipoprotein E4 carriers
published pages: , ISSN: 2632-1297, DOI: 10.1093/braincomms/fcz003
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