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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.

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

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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