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ALZSYN SIGNED

Imaging synaptic contributors to dementia

Total Cost €

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EC-Contrib. €

0

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.

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

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

Leaflet | Map data © OpenStreetMap contributors, CC-BY-SA, Imagery © Mapbox

 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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