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ALZSYN SIGNED

Imaging synaptic contributors to dementia

Total Cost €

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EC-Contrib. €

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Partnership

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 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.

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

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 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

year authors and title journal last update
List of publications.
2019 Marta Querol-Vilaseca, Martí Colom-Cadena, Jordi Pegueroles, Raúl Nuñez-Llaves, Joan Luque-Cabecerans, Laia Muñoz-Llahuna, Jordi Andilla, Olivia Belbin, Tara L. Spires-Jones, Ellen Gelpi, Jordi Clarimon, Pablo Loza-Alvarez, Juan Fortea, Alberto Lleó
Nanoscale structure of amyloid-β plaques in Alzheimer’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 Alzheimer’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.

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