IMMUNE/MEMORY AGING

Can immune system rejuvenation restore age-related memory loss?

 Coordinatore WEIZMANN INSTITUTE OF SCIENCE 

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 Nazionalità Coordinatore Israel [IL]
 Totale costo 1˙650˙000 €
 EC contributo 1˙650˙000 €
 Programma FP7-IDEAS-ERC
Specific programme: "Ideas" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013)
 Code Call ERC-2008-AdG
 Funding Scheme ERC-AG
 Anno di inizio 2009
 Periodo (anno-mese-giorno) 2009-01-01   -   2012-12-31

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    WEIZMANN INSTITUTE OF SCIENCE

 Organization address address: HERZL STREET 234
city: REHOVOT
postcode: 7610001

contact info
Titolo: Ms.
Nome: Talia
Cognome: Tzahor
Email: send email
Telefono: -3996
Fax: -6079

IL (REHOVOT) hostInstitution 1˙650˙000.00
2    WEIZMANN INSTITUTE OF SCIENCE

 Organization address address: HERZL STREET 234
city: REHOVOT
postcode: 7610001

contact info
Titolo: Prof.
Nome: Michal
Cognome: Eisenbach-Schwartz
Email: send email
Telefono: -2437
Fax: -5988

IL (REHOVOT) hostInstitution 1˙650˙000.00

Mappa


 Word cloud

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immune    related    brain    immunity    decline    elderly    aging    sufficient    self    cognition    therapies    contributes    plasticity    life    cell    cognitive    hippocampal    age    memory    loss    reversible   

 Obiettivo del progetto (Objective)

'With increased life expectancy, there has been a critical growth in the portion of the population that suffers from age-related cognitive decline and dementia. Attempts are therefore being made to find ways to slow brain-aging processes; successful therapies would have a significant impact on the quality of life of individuals, and decrease healthcare expenditures. Aging of the immune system has never been suggested as a factor in memory loss. My group formulated the concept of protective autoimmunity , suggesting a linkage between immunity and self-maintenance in the context of the brain in health and disease. Recently, we showed that T lymphocytes recognizing brain-self antigens have a pivotal role in maintaining hippocampal plasticity, as manifested by reduced neurogenesis and impaired cognitive abilities in T-cell deficient mice. Taken together, our novel observations that T cell immunity contributes to hippocampal plasticity, and the fact that T cell immunity decreases with progressive aging create the basis for the present proposal. We will focus on the following questions: (a) Which aspects of cognition are supported by the immune system- learning, memory or both; (b) whether aging of the immune system is sufficient to induce aging of the brain; (c) whether activation of the immune system is sufficient to reverse age-related cognitive decline; (d) the mechanism underlying the effect of peripheral immunity on brain cognition; and (e) potential therapeutic implications of our findings. Our preliminary results demonstrate that the immune system contributes to spatial memory, and that imposing an immune deficiency is sufficient to cause a reversible memory deficit. These findings give strong reason for optimism that memory loss in the elderly is preventable and perhaps reversible by immune-based therapies; we hope that, in the not too distant future, our studies will enable development of a vaccine to prevent CNS aging and cognitive loss in elderly.'

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