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URBACH-ALZ

Hyper-emotionality after neurodegenerative loss of inhibition of the amygdala

Total Cost €

0

EC-Contrib. €

0

Partnership

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 URBACH-ALZ project word cloud

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

animals    signaling    causal    caused    ot    damage    chemogenetic    town    plan    inhibitory    causally    neurobiological    anatomical    settlers    reported    central    mutation    construct    bilateral    uniquely    neurodegeneration    profiles    treat    cerebrospinal    university    decreased    host    urbach    alzheimer    function    translational    amygdala    adding    chemogenetically    lausanne    behavioral    patients    rare    basis    south    causes    cape    worldwide    attached    handful    400    clinical    cea    genetic    wie    uwd    firm    model    fear    found    group    decrease    projections    insecurely    collaborators    lab    hypothesis    attachment    stronger    gt    center    correlating    ad    bla    tests    oxytocin    onto    deeper    dutch    hyper    individuals    occurring    blood    disorders    gained    functional    relation    anxiety    animal    anc    multidisciplinary    special    started    disease    basolateral    human    mri    spread    give    personality    levels    africa    opto    fluid    hypothesize   

Project "URBACH-ALZ" data sheet

The following table provides information about the project.

Coordinator
FONDAZIONE ISTITUTO ITALIANO DI TECNOLOGIA 

Organization address
address: VIA MOREGO 30
city: GENOVA
postcode: 16163
website: www.iit.it

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 Italy [IT]
 Total cost 173˙634 €
 EC max contribution 173˙634 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2015
 Funding Scheme MSCA-IF-EF-ST
 Starting year 2017
 Duration (year-month-day) from 2017-01-01   to  2018-12-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    FONDAZIONE ISTITUTO ITALIANO DI TECNOLOGIA IT (GENOVA) coordinator 42˙069.00
2    CENTRE HOSPITALIER UNIVERSITAIRE VAUDOIS CH (LAUSANNE) participant 131˙564.00

Map

 Project objective

'I propose to test how hyper-anxiety in Alzheimer's disease (AD) patients is caused by neurodegeneration in the amygdala, our 'center of fear', by comparing with a unique group of Urbach Wiethe disease (UWD) patients with bilateral neurodegeneration of the amygdala (BLA) for which I also construct an animal model. UWD is caused by a very rare genetic mutation occurring in only a handful of individuals worldwide. My host in Lausanne has gained access, however, to a uniquely large group of UWD patients in South-Africa (>40) where the mutation has spread for 400 years in Dutch settlers. Our collaborators at Cape Town University have found, in anatomical & functional MRI and special behavioral tests, how specific loss of inhibitory projections from the basolateral (BLA) onto the central part of the amygdala (CeA) causes hyper-anxiety in UWD. Based upon recently reported BLA neurodegeneration in AD patients, I hypothesize a crucial BLA role in hyper-anxiety of AD patients. I plan to test this in AD patients with clinical collaborators in Lausanne and, to test this hypothesis causally, I have started to opto,- anc chemogenetically decrease BLA function in an animal model. In addition, in Lausanne a stronger hyper-anxiety was observed in AD patients with insecurely attached personality profiles. As my host lab has established an inhibitory role of oxytocin (OT) in the CeA, I hypothesize a decreased OT signaling in CeA of these patients, adding to the anxiety already caused by the BLA loss. I plan to test this both in AD and UWD patients by correlating attachment profiles with OT levels (in blood & cerebrospinal fluid) and anxiety levels & BLA damage (MRI). I will use opto&chemogenetic targeting of OT signaling in animals for a causal relation. This multidisciplinary and translational approach can give a deeper understanding of the role of the amygdala in hyper-anxiety in human patients, and provide a firm neurobiological basis for applying OT to treat anxiety disorders. '

 Publications

year authors and title journal last update
List of publications.
2018 David Terburg, Diego Scheggia, Rodrigo Triana del Rio, Floris Klumpers, Alexandru Cristian Ciobanu, Barak Morgan, Estrella R. Montoya, Peter A. Bos, Gion Giobellina, Erwin H. van den Burg, Beatrice de Gelder, Dan J. Stein, Ron Stoop, Jack van Honk
The Basolateral Amygdala Is Essential for Rapid Escape: A Human and Rodent Study
published pages: 723-735.e16, ISSN: 0092-8674, DOI: 10.1016/j.cell.2018.09.028
Cell 175/3 2019-08-30

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