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Guest lectures by Claudio Franceschi
Claudio Franceschi, distinguished gerontologist and head
of the Interdepartmental Centre “L. Galvani” for
the Study of Biocomplexity, University of Bologna, Italy,
will be visiting Norway 2 - 5 March 2004. During his stay,
which is co-hosted by Prof. Erling Seeberg, Centre for Molecular
Biology and Neuroscience, Oslo, and Prof. Stig W. Omholt,
CIGENE, Ås, he will give two talks, one in Oslo and
one in Ås.
Professor Franceschi is a world leading capacity within
Aging Research and has been working with a unique material
of centenarians in Italy. He is the Scientific Director of
the Italian National Research Centre on Ageing, Ancona, Italy.
Prof. Claudio Franceschi, Interdepartmental Center “L.
Galvani” for the study of Biocomplexity , University of Bologna,
Italy, will give a guest lecture on Thursday 4 March 2004 at
14:00 in auditorium A3.3067 at Molecular Microbiology, Rikshospitalet,
with
the title:
Immunology and genetics of ageing and longevity
in humans
The ultimate goal of the biomedical research on aging is to
improve the health status of elderly people, identifying risk
factors for frailty, disability and major age-related diseases.
Thus, the research on aging should be focussed on human aging
but this type of research has tremendous limitations, owing to
the complexity of human lifespan determinants, the interaction
between Nature and Culture, and the strong ethical implications.
Nevertheless, we will try to show that the study of human aging
and longevity can disclose perspectives which have not been predicted
by the study of model systems such as C. elegans, D.
melanogaster,
and M. musculus. To this purpose the results of epidemiological/demographic
studies on centenarians (Sardinia, Mantova province) will be
illustrated, with particular attention to gender difference and
the non-random geographic distribution of centenarians. Important
but neglected topics such as quality and quantity of sleep in
very old people will be addressed. As far as the biological determinants
of longevity are concerned, we will focus on the hypothesis that
chronic antigenic load represents one of the major driving force
of the rate of aging and of the onset of major age-related diseases,
being responsible for INFLAMM-AGEING, i.e. the peculiar chronic
inflammatory status, which develops with age in humans and is
involved in frailty and sarcopenia. Starting from data on IGF-1
plasma levels and its genetic control in nonagenarians and centenarians
we will argue that in old people a trade-off likely exists between
maintenance of muscle mass and strength and cancer incidence,
suggesting that one of the major finding which emerged from studies
in animal models, i.e. the importance for longevity of insulin/IGF-1–signaling
pathway, likely has a counterpart in humans. This pathway is
involved in glucose and energy utilisation, two metabolic activities
in which mitochondria play a central role. We will present data
suggesting that a complex interplay between nuclear and mitochondrial
genomes occurs, and that germ line mitochondrial DNA variants
and mutations likely affect human longevity. Finally, we will
discuss the urgency of an integrated approach and the need of
innovative theoretical models, encompassing the major environmental
and biological variables, which are known to contribute to ageing
and longevity, in order to disentangle the complexity of these
phenomena in animal models as well as in humans.
Prof. Franceschi will also give a guest lecture
on Wednesday 3 March 2004 at 1115-1200 in auditorium
U338 in "Urbygningen" at the Agricultural University
of Norway at Ås, with the title:
The immune system as a complex system: mathematical
models of immunosenescence
The general architecture of the immune system as a complex system
involving billions of interacting cells and molecules will be
illustrated paying particular attention to the evolutionary moulded
interaction between innate and clonotypical immunity. It will
be illustrated how a specific immune response to a particular
epitope emerges from a structural background characterized by
a high degeneracy and promiscuity of receptors and ligands. The
hypothesis will be pursued that the changes that the immune system
undergoes on a long temporal scale (immunosenescence) allow to
understand additional characteristics of the system, and particularly
the role that chronic antigenic load and “immunological
noise” can play in maintaining immunological memory. Two
mathematical models regarding this last topic will be illustrated.
Information from AUN
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