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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.

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

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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