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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.

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

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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