Thursday, January 24, 2008

Cell Article on Mitochondria and Aging

As I've noted several times before (see here, here and here), a great deal of my current research concerns the moral imperative to retard human aging. This is a truly fascinating topic to examine. When I tell people I am working on this topic they react in different and interesting ways. "Could we actually do this?" "Would we want to do this?" Few topics can enliven a dull dinner party like a discussion of the ethical and social implications of aging research! And I believe that moral and political philosophers should be investing a greater portion of their energies into tackling these important and timely issues.

The latest issue of Cell has a fascinating essay by Leonard Guarente entitled "Mitochondria—A Nexus for Aging, Calorie Restriction, and Sirtuins?". This essay is a great example of the truly amazing advances that are being made in our understanding of the biology of aging. And this scientific research could lead to interventions that confer enormous health benefits. Here is the abstract:

Recent studies of calorie restriction in several organisms demonstrate an increase in mitochondrial activity that is associated with the salutary effects of this dietary restriction regimen. In this Essay, I speculate on how an increase in mitochondrial activity might provide benefit and discuss how diet, mitochondria, and sirtuins might interact in a pathway to slow aging and associated diseases.

And a sample from the Essay:

Mitochondria have long been proposed to play an important role in aging. Recent genetic findings in lower organisms have pinpointed sirtuins as antiaging genes, and at least four of the seven mammalian sirtuin homologs have mitochondria-associated functions. CR is perhaps the most robust intervention that extends mammalian life span and has been associated with an increase in SIRT1 levels in several tissues and a corresponding increase in mitochondrial components. Here, I have presented several models for how this increase in mitochondria may have the effect of slowing aging and disease. Some of the models rely on an important role of ROS in the aging process, whereas others do not. It is hoped that the next few years will see a further convergence of genetic pathways with mitochondrial function, which will provide a comprehensive view of aging and antiaging mechanisms and will also explain how CR works. It seems likely that we are on the right track of acquiring this understanding, and that it will involve mechanisms rich in new and old ideas about aging and how to counteract it.