MEMOSAD

Memory loss in Alzheimer disease: underlying mechanisms and therapeutic targets

 Coordinatore VERUM- STIFTUNG FUER VERHALTEN UND UMWELT 

 Organization address address: THERESIENSTRASSE 6-8
city: MUENCHEN
postcode: 80333

contact info
Titolo: Prof.
Nome: Franz
Cognome: Adlkofer
Email: send email
Telefono: -5309920
Fax: -53098869

 Nazionalità Coordinatore Germany [DE]
 Sito del progetto http://www.verum-foundation.de/memosad
 Totale costo 4˙023˙079 €
 EC contributo 2˙998˙696 €
 Programma FP7-HEALTH
Specific Programme "Cooperation": Health
 Code Call FP7-HEALTH-2007-A
 Funding Scheme CP-FP
 Anno di inizio 2008
 Periodo (anno-mese-giorno) 2008-01-01   -   2011-06-30

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    VERUM- STIFTUNG FUER VERHALTEN UND UMWELT

 Organization address address: THERESIENSTRASSE 6-8
city: MUENCHEN
postcode: 80333

contact info
Titolo: Prof.
Nome: Franz
Cognome: Adlkofer
Email: send email
Telefono: -5309920
Fax: -53098869

DE (MUENCHEN) coordinator 0.00
2    ALBERT-LUDWIGS-UNIVERSITAET FREIBURG

 Organization address address: FAHNENBERGPLATZ
city: FREIBURG
postcode: 79085

contact info
Titolo: Ms.
Nome: Gabriela
Cognome: Hafke-Wessel
Email: send email
Telefono: -2035079
Fax: -2039578

DE (FREIBURG) participant 0.00
3    KATHOLIEKE UNIVERSITEIT LEUVEN

 Organization address address: Oude Markt 13
city: LEUVEN
postcode: 3000

contact info
Titolo: Ms.
Nome: Marion
Cognome: Wolpers
Email: send email
Telefono: -326504
Fax: -326499

BE (LEUVEN) participant 0.00
4    LUDWIG-MAXIMILIANS-UNIVERSITAET MUENCHEN

 Organization address address: GESCHWISTER SCHOLL PLATZ 1
city: MUENCHEN
postcode: 80539

contact info
Titolo: Mr.
Nome: Mathias
Cognome: Becker
Email: send email
Telefono: -21803645
Fax: -21803025

DE (MUENCHEN) participant 0.00
5    MAX PLANCK GESELLSCHAFT ZUR FOERDERUNG DER WISSENSCHAFTEN E.V.

 Organization address address: Hofgartenstrasse 8
city: MUENCHEN
postcode: 80539

contact info
Titolo: Ms.
Nome: Elke
Cognome: Spader
Email: send email
Telefono: -89982793
Fax: -89716801

DE (MUENCHEN) participant 0.00
6    SENEXIS LTD

 Organization address address: Babraham Research Campus
city: CAMBRIDGE
postcode: CB22 3AT

contact info
Titolo: Dr.
Nome: Mark
Cognome: Treherne
Email: send email
Telefono: -497339
Fax: -497340

UK (CAMBRIDGE) participant 0.00
7    UNIVERSITAT AUTONOMA DE BARCELONA

 Organization address address: Campus UAB -BELLATERRA- s/n
city: CERDANYOLA DEL VALLES
postcode: 8193

contact info
Titolo: Ms.
Nome: Katja
Cognome: Schustakowitz
Email: send email
Telefono: -5812999
Fax: -5812082

ES (CERDANYOLA DEL VALLES) participant 0.00
8    UNIVERSITE DE LILLE II - DROIT ET SANTE

 Organization address address: RUE PAUL DUEZ 42
city: Lille
postcode: 59800

contact info
Titolo: Dr.
Nome: Marie
Cognome: Gompel
Email: send email
Telefono: -20965185
Fax: -20965193

FR (Lille) participant 0.00
9    UNIVERSITY COLLEGE DUBLIN, NATIONAL UNIVERSITY OF IRELAND, DUBLIN

 Organization address address: BELFIELD
city: DUBLIN
postcode: 4

contact info
Titolo: Mr.
Nome: Donal
Cognome: Doolan
Email: send email
Telefono: -7161304
Fax: -7160864

IE (DUBLIN) participant 0.00
10    VIB

 Organization address address: Rijvisschestraat 120
city: ZWIJNAARDE - GENT
postcode: 9052

contact info
Titolo: Mr.
Nome: Wim
Cognome: Goemaere
Email: send email
Telefono: -2446588
Fax: -2446587

BE (ZWIJNAARDE - GENT) participant 0.00

Mappa


 Word cloud

Esplora la "nuvola delle parole (Word Cloud) per avere un'idea di massima del progetto.

alzheimer    forms    synaptotoxicity    pathologic    mechanism    therapeutic    mechanisms    accumulation    disease    mouse    function    cultures    insoluble    proteins    aggregates    employed    functional    models    largely    toxicity    scientists    primary    memosad    demonstrated    cognitive    synaptic    triggers    health    pathology    suggest    tau    neuronal    treating    memory    neurons    animal    validated    unknown    impairment    dysfunction    toxic    pathways    aggregation    ad    pathologies    dementia    abeta    molecular    loss    pathological    related    species   

 Obiettivo del progetto (Objective)

'MEMOSAD aims at defining the molecular mechanisms of Abeta- and Tau-induced synaptotoxicity and at developing disease-modifying therapeutics for the prevention of memory loss in Alzheimer disease (AD). Insoluble aggregates of the two proteins provide the pathological hallmarks of this incurable brain disorder. Early stage AD is characterized by a remarkably pure impairment of declarative memory and several lines of evidence suggest that this memory impairment is independent of the insoluble aggregates, does not require neuronal death and is caused by subtle and transient synaptic changes. The toxic Abeta and Tau species that cause synaptic dysfunction, their mechanism of toxicity and the link between both pathologies remain largely unknown, but recent data suggest that Abeta accumulation triggers Tau pathology. Consequently, primary neuronal cultures and animal models (C.elegans,zebrafish,mouse) will be employed to define the pathologic pathways leading from Abeta through Tau to synaptotoxicity. Initial experiments will investigate the effect of well-defined Abeta species on long term potentiation, synaptic morphology, gene expression, Tau phosphorylation/aggregation, axonal transport and behaviour. Similarly, we will investigate the functional consequences of Tau misfunction, aggregation, hyperphosphorylation and missorting in various cell culture systems (retinal ganglion cells, primary hippocampal neurons, organotypical slices) and animal models, especially with regard to intraneuronal trafficking and synaptic function. Once the toxic Abeta and Tau species are known and their mechanism of toxicity are defined, we will investigate how these pathways interact. Unravelling the pathologic pathways that lead from Abeta through Tau to synaptotoxicity and memory loss should reveal novel points for therapeutic intervention. Our aim is to deliver 3 or 4 validated therapeutic targets and at least 2 compounds with demonstrated therapeutic efficacy in mouse models of AD.'

Introduzione (Teaser)

Two proteins play an instrumental role in the cognitive deficit associated with Alzheimer's disease (AD) and other forms of dementia. EU-funded scientists have now developed targeted therapies with great promise for millions of sufferers.

Descrizione progetto (Article)

Memory is largely mediated by signalling between neurons at synapses, the location where neurons are in very close conjunction with each other. Synaptic dysfunction thus plays a role in memory loss commonly seen in most forms of dementia and is a hallmark of AD.

On a molecular level, AD is characterised by abnormal insoluble aggregates of two proteins, the amyloid-beta peptide (Abeta) and tau. The former contributes to extracellular neuritic plaques, and the latter to intracellular neurofibrillary tangles. Pathological changes in AD suggest that Abeta accumulation triggers tau pathology, but mechanisms are largely unknown.

Scientists initiated the EU-funded project 'Memory loss in Alzheimer disease: Underlying mechanisms and therapeutic targets' (MEMOSAD) to identify the toxic Abeta and tau species, their mechanisms of toxicity and their interrelationship. The ultimate goal was identification of potential therapeutic targets to combat the devastating and irreversible memory loss in AD and related pathologies.

Researchers employed commonly used primary neuronal cultures and animal models to untangle the mystery. They investigated the effects of well defined Abeta species and the functional consequences of aberrant tau processing and aggregation on a number of molecular substrates of synaptic function.

MEMOSAD members collaborated to successfully generate Abeta aggregation inhibitors and demonstrated memory improvements in two rodent models. Scientists also validated the use of tau immunotherapy in treating AD and other tau-related pathologies. Results showed a reduction in aggregated tau and a delay in the onset of cognitive deficits following immunisation.

The identified targets represent an important breakthrough in treating or slowing the progression of AD. This may also prove to be a valuable diagnostic tool or biomarker for AD, other forms of dementia and related neurodegenerative disorders such as Parkinson's disease. AD and dementia are global public health priorities. MEMOSAD has made a significant contribution to ameliorating their impact on the lives of patients, caregivers and overburdened health care systems.

Altri progetti dello stesso programma (FP7-HEALTH)

EDUFLUVAC (2013)

Combinatorial immunization strategy to educate the immune system towards cross recognition and coverage against antigenic drift in seasonal influenza virus exposure

Read More  

RAPTADIAG (2012)

Rapid Aptamer based diagnostics for bacterial meningitis

Read More  

ENERGY (2009)

EuropeaN Energy balance Research to prevent excessive weight Gain among Youth

Read More