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ALZSYN SIGNED

Imaging synaptic contributors to dementia

Total Cost €

EC-Contrib. €

Partnership

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Outcomes and
results

ALZSYN project word cloud

Explore the words cloud of the ALZSYN project. It provides you a very rough idea of what is the project "ALZSYN" about.

despite cutting 99 experiments decline suggests disease accepted ultimately pathological function neurons recovery mechanistic clinical treat integrating imaging decade cascade people drugs devastating older plays neural combine strongest techniques care cell synapses 6 crisis dysfunction synapse tomography breaking brain familial proteome ages public restore team pathology stem correlate alterations tau therapeutic progress trials cognitive critical begins unmet ground relevance neurodegeneration human circuit therapeutics modifying expressing intervening array impairment health mechanisms hypothesis downstream multiphoton initiate population lost model attempting amyloid causing dementia edge beta degeneration rate collapse models unclear intervention confirm postmortem structure mounting alzheimer

Project "ALZSYN" data sheet

The following table provides information about the project.

Coordinator	THE UNIVERSITY OF EDINBURGH Organization address address: OLD COLLEGE, SOUTH BRIDGE city: EDINBURGH postcode: EH8 9YL website: www.ed.ac.uk contact info title: n.a. name: n.a. surname: n.a. function: n.a. email: n.a. telephone: n.a. fax: n.a.
Coordinator Country	United Kingdom [UK]
Project website	https://www.pure.ed.ac.uk/admin/editor/dk/atira/pure/modules/unifiedprojectmodel/external/model/project/editor/upmprojecteditor.xhtml
Total cost	2˙000˙000 €
EC max contribution	2˙000˙000 € (100%)
Programme	1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
Code Call	ERC-2015-CoG
Funding Scheme	ERC-COG
Starting year	2016
Duration (year-month-day)	from 2016-11-01 to 2021-10-31

Partnership

Take a look of project's partnership.

#	participants	country	role	EC contrib. [€]
1	THE UNIVERSITY OF EDINBURGH THE UNIVERSITY OF EDINBURGH Organization address address: OLD COLLEGE, SOUTH BRIDGE city: EDINBURGH postcode: EH8 9YL website: www.ed.ac.uk contact info title: n.a. name: n.a. surname: n.a. function: n.a. email: n.a. telephone: n.a. fax: n.a.	UK (EDINBURGH)	coordinator	2˙000˙000.00

Map

Project objective

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.

Publications

List of publications.
year	authors and title	journal	last update
2019	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
2017	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	Synapse 71/6	2020-01-24
2019	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	Brain Communications	2020-01-24

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The information about "ALZSYN" are provided by the European Opendata Portal: CORDIS opendata.