IMMUNE/MEMORY AGING

Can immune system rejuvenation restore age-related memory loss?

Coordinatore	WEIZMANN INSTITUTE OF SCIENCE    more Spiacenti, non ci sono informazioni su questo coordinatore. Contattare Fabio per maggiori infomrazioni, grazie.
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

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 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.'