Opendata, web and dolomites
  1. home
  2. trasparenza
  3. open h2020
  4. urbach-alz

URBACH-ALZ

Hyper-emotionality after neurodegenerative loss of inhibition of the amygdala

Total Cost €

0

EC-Contrib. €

0

Partnership

0

Views

0
 Outcomes and results

 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.

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

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

Are you the coordinator (or a participant) of this project? Plaese send me more information about the "URBACH-ALZ" project.

For instance: the website url (it has not provided by EU-opendata yet), the logo, a more detailed description of the project (in plain text as a rtf file or a word file), some pictures (as picture files, not embedded into any word file), twitter account, linkedin page, etc.

Send me an  email (fabio@fabiodisconzi.com) and I put them in your project's page as son as possible.

Thanks. And then put a link of this page into your project's website.

The information about "URBACH-ALZ" are provided by the European Opendata Portal: CORDIS opendata.

More projects from the same programme (H2020-EU.1.3.2.)

MIMIC (2020)

Deciphering how microbiota modulate anti-tumor immune responses in checkpoint therapy

Read More  

BiMetaCat (2019)

Two Are Better Than One: Bimetallic Catalysts for the Conversion of Lignin-Derived Aryl-Ethers

Read More  

LYSOKIN (2020)

Architecture and regulation of PI3KC2β lipid kinase complex for nutrient signaling at the lysosome

Read More