Towards a systems view of aging

On several occasions both in this blog and in my treatise I have pointed out the need for integrating the various disparate theories of aging into an overall systems framework.  Following is the abstract for a presentation I will be offering at the American Aging Association’s 39th Annual Meeting and 24th Annual Meeting of the American College of Clinical Gerontology in Portland Oregon June 4-7, 2010:

Towards a systems view of aging

A comprehensive systems theory of aging must embrace the validated teachings of multiple existing special theories of aging, theories that range from oxidative damage to loss of mitochondrial function to neurological degeneration to telomere shortening and cell senescence to decline in hormone levels.  The author has characterized 14 such major theories and an additional 7 candidate ones.   While each such theory is correct in its own framework of reference, on the surface most seem to be largely independent of the others.  However, on the levels of molecular biology and genomics a rich network of links exists among these theories.  The author suggests two overarching frameworks for integrating and clarifying existing understandings from the diverse theories of aging.  One framework is lifelong programmed changes in global gene expression due to DNA methylation, histone acetylation and other epigenomic modifications.  For example, aging-related decline of efficacy of DNA repair machinery might possibly result from promoter methylation of the Mms22 gene, resulting in increasing susceptibility to oxidative damage with age.  Promoter methylation of the P21 and P53 apoptosis genes can result in increased susceptibility to cancers.  The second framework sees aging as decline in functioning of the stem cell supply chain, the chain where adult stem and progenitor cells progressively differentiate as-needed into other cells of increased specificity and decreased pluripotency, resulting in lifelong renewal of somatic cell types.  As the supplies of multipotent mesenchymal and haemopoietic stem cells available in their niches for differentiation decline because of their replicative senescence, for example, fewer progenitor and somatic cells are available to replace ones that have died or become senescent.  The paper will embody insights developed over a multi-year period and described in the author’s online treatise ANTI-AGING FIREWALLS – THE SCIENCE AND TECHNOLOGY OF LONGEVITY and in the hundreds of postings in the author’s blog

In the course of the next couple of weeks I expect to produce a more detailed version of that presentation for this blog.

About Vince Giuliano

Being a follower, connoisseur, and interpreter of longevity research is my latest career. I have been at this part-time for well over a decade, and in 2007 this became my mainline activity. In earlier reincarnations of my career. I was founding dean of a graduate school and a university professor at the State University of New York, a senior consultant working in a variety of fields at Arthur D. Little, Inc., Chief Scientist and C00 of Mirror Systems, a software company, and an international Internet consultant. I got off the ground with one of the earliest PhD's from Harvard in a field later to become known as computer science. Because there was no academic field of computer science at the time, to get through I had to qualify myself in hard sciences, so my studies focused heavily on quantum physics. In various ways I contributed to the Computer Revolution starting in the 1950s and the Internet Revolution starting in the late 1980s. I am now engaged in doing the same for The Longevity Revolution. I have published something like 200 books and papers as well as over 430 substantive.entries in this blog, and have enjoyed various periods of notoriety. If you do a Google search on Vincent E. Giuliano, most if not all of the entries on the first few pages that come up will be ones relating to me. I have a general writings site at and an extensive site of my art at Please note that I have recently changed my mailbox to
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2 Responses to Towards a systems view of aging

  1. admin says:

    Hi Vincent
    I did look at the article. It is a very strange case of physical development arrest. Study of this case may tell us something about early-stage aging as related to development but my guess is that it is unlikely to tell us much about post-maturity aging or how lives may be extended. The obvious point is that there is an aging program that starts with conception. Verious bugs in the aging program can impede normal development to maturity, as in the case of the boy described in the article. While many researchers do not think there is an aging program that continues after maturity, several including myself think that in effect there is one or several. In my treatise I have discussed two frameworks for such a program, Programmed Epigenomic Changes and Stem Cell Supply Chain Breakdown.


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