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TOLKEDA SIGNED

Modulating brain structural plasticity versus neurodegeneration via a novel mechanism involving neurotrophins and dopamine, Tolls and Kek truncated-Trk-like receptors in Drosophila.

Total Cost €

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EC-Contrib. €

0

Partnership

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 TOLKEDA project word cloud

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

ro3    preliminary    drives    population    gene    dnt    expert    ageing    neurotrophin    principal    neuromodulator    ros    tolls    circuit    grow    mechanism    operates    adult    costing    dopaminergic    dopamine    neurodegeneration    sun    ro2    models    larvae    disease    module    synaptic    editing    vs    researcher    imperative    molecular    plasticity    pd    life    formed    brain    burden    adapt    tolkeda    incidence    trk    altering    model    hidalgo    maintains    truncated    homeostasis    treat    discover    kek    neuroprotection    diseases    neurotrophins    alicia    map    neurological    causes    cardiovascular    pi    synapses    signalling    linked    deficits    toll    receptors    hypothesis    shows    dr    neural    registration    cancer    underlies    ro1    parkinson    behavioural    jun    er    modulates    put    dnts    ages    health    drosophila    overlapping    neuronal    discovered    neurites    neurodegenerative    elimination    functions    synergy    dans    linking    generation    demonstrated    neurons    manipulating    structural    create    provoke    investigator    degeneration   

Project "TOLKEDA" data sheet

The following table provides information about the project.

Coordinator
THE UNIVERSITY OF BIRMINGHAM 

Organization address
address: Edgbaston
city: BIRMINGHAM
postcode: B15 2TT
website: www.bham.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]
 Total cost 195˙454 €
 EC max contribution 195˙454 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2017
 Funding Scheme MSCA-IF-EF-ST
 Starting year 2018
 Duration (year-month-day) from 2018-08-01   to  2020-07-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    THE UNIVERSITY OF BIRMINGHAM UK (BIRMINGHAM) coordinator 195˙454.00

Map

 Project objective

The aim of TOLKEDA is to test the hypothesis that a novel molecular mechanism linking neurotrophins, Tolls and truncated Trk-like receptors modulates structural brain plasticity vs. neurodegeneration. The brain changes throughout life: structural plasticity drives generation of neurites, neurons and synapses to adapt and learn; their elimination maintains homeostasis, but causes neurodegeneration in ageing and disease. Brain disease is the major health burden in Europe, costing more than cancer and cardiovascular diseases put together, and its incidence will grow as the population ages. It is imperative to discover novel molecular pathways that can be targeted to treat brain disease. The Principal Investigator (PI) Dr Alicia Hidalgo recently discovered a novel Drosophila neurotrophin (DNT) mechanism formed of neurotrophins, Toll and truncated-Trk-like receptors, and demonstrated that it underlies neuronal number and synaptic structural plasticity in larvae. Preliminary evidence shows that the DNT system operates in the adult brain, overlapping with dopaminergic neurons (DANs). Dopamine is a key neuromodulator, and degeneration of DANs underlies neurological and neurodegenerative diseases, such as Parkinson’s disease (PD). The Experienced Researcher (ER), Jun Sun, is an expert in the dopaminergic system and Drosophila PD models. The timely collaboration between PI and ER will provoke synergy to address effectively the following research objectives (ROs): RO1: to create a map of DNTs, Toll-6, Kek-6 and DANs in the adult brain, using gene editing technology and neural circuit registration. RO2: to test whether altering the functions of DNTs, Toll-6 and Kek-6 causes structural brain deficits, including in the dopaminergic system, and whether they are linked to behavioural deficits and neuronal activity. RO3: to test whether manipulating the DNT/Toll-6/Kek-6 signalling module in the dopaminergic system can promote neuroprotection in a Drosophila PD model.

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

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