PROFITS

Bridging the world of fungi and dementia

Coordinatore	TECHNISCHE UNIVERSITAT BERLIN    more  Organization address address: STRASSE DES 17 JUNI 135 city: BERLIN postcode: 10623 contact info Titolo: Ms. Nome: Simone Cognome: Ludwig Email: send email Telefono: +49 30 314 21371 Fax: +49 30 314 21689
Nazionalità Coordinatore	Germany [DE]
Totale costo	100˙000 €
EC contributo	100˙000 €
Programma	FP7-PEOPLE Specific programme "People" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013)
Code Call	FP7-PEOPLE-2011-CIG
Funding Scheme	MC-CIG
Anno di inizio	2012
Periodo (anno-mese-giorno)	2012-02-01   -   2016-01-31

 Partecipanti

#	participant	country	role	EC contrib. [€]
1	TECHNISCHE UNIVERSITAT BERLIN  Organization address address: STRASSE DES 17 JUNI 135 city: BERLIN postcode: 10623 contact info Titolo: Ms. Nome: Simone Cognome: Ludwig Email: send email Telefono: +49 30 314 21371 Fax: +49 30 314 21689	DE (BERLIN)	coordinator	100˙000.00

Mappa

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 Obiettivo del progetto (Objective)

'Alzheimer’s disease is the most common form of dementia which seriously interferes with the daily life of millions of people. People suffering from Alzheimer’s disease show the accumulation of two misfolded proteins in the nerve cells of their brains – amyloid plaques and tau tangles. Although many aspects of the Alzheimer’s disease pattern are well-established, only little is known about the onset, development and progression of this disease. Thus, early detection, including diagnosis before symptoms become visible, is still not possible yet. Furthermore, the development of drugs designed to slow down or even prevent Alzheimer’s disease progression is very difficult and tedious. In the envisaged project, a microorganism, the filamentous fungus Aspergillus niger, will be used to study the onset and development of Alzheimer’s disease. The presence of misfolded proteins in this microorganism provokes a cellular reaction that shows many parallels to what is known from nerve cells. It seems that both man and fungus use similar defense strategies to detect and get rid of dangerous misfolded proteins. This makes A. niger very appealing for use as a model system to explore in utmost detail the origin and temporal progression of Alzheimer’s disease. As it is a fast-growing and easy genetically tractable organism, respective analyses can be performed very cost and time effective, something which is not feasible when working with human cell models.'