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Imaging synaptic contributors to dementia

Total Cost €


EC-Contrib. €






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

Project "ALZSYN" data sheet

The following table provides information about the project.


Organization address
postcode: EH8 9YL

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
 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


Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    THE UNIVERSITY OF EDINBURGH UK (EDINBURGH) coordinator 2˙000˙000.00


 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.


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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