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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.

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

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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