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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.

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

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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