Via Ouroboros and a few other places, I note that the open-access journal PLoS Genetics has started off on a series of reviews and opinion pieces on aging science.
In keeping with the mission statement of our journal to present interdisciplinary research in the broadest possible context, we have commissioned a series of Review and Opinion articles bound thematically to a discrete set of topics of inherent complexity, as well as broad interest. Each component of the series will examine a facet of the chosen problem and we hope that the amalgam of each series, which will be available electronically as a unified entity, will both educate the non-specialist as well as provide a balanced view that will transmit to our readership an appreciation of the progress made and the future trends in each field.
Our inaugural series focuses on aging, a field under both rapid evolution and substantial controversy.
Yes indeed - though the focus here skirts around the most interesting controversy of all, that surrounding the moral imperative to apply scientific knowledge to treat, repair and otherwise cure aging as soon as possible. There is considerable controversy and ongoing change within and surrounding the gerontology community on topics such as the potential timescales of extending healthy longevity, and whether that goal should be the focus of research.
(My point of view: what is the point of researching a field of medicine that relates to great suffering, pain and death if not to as rapidly as possible use that knowledge to prevent that suffering, pain and death? Aging is no different from cancer or AIDS in that respect, and you don't hear many voices within the cancer research community advocating a "look but don't touch" philosophy of science).
The first review in the series is a topic long-time readers might be familiar with; an examination of the nuts and bolts of the mitochondrial free radical theory of aging, such as it is understood today.
The mitochondrial theory of aging is based on the premise that reactive oxygen species (ROS), generated throughout the lifespan of an organism, damage mitochondrial macromolecules, including proteins, lipids, and mtDNA. Although most molecular damage is reversible through repair or molecular turnover mechanisms, unrepaired DNA damage may lead to mutations that accumulate as a function of age. The accumulation of mutations ultimately leads to permanent age-related mitochondrial dysfunction, which contributes to the aging phenotype.
The precise nature of the details are still being debated; the plausible scenario put forward by biomedical gerontologist Aubrey de Grey a few years back (and explained for the layman in a past post here at Fight Aging!) is still not an open and shut case at this time. Bulletproof analysis of the evolution of very complex biochemical systems across years and decades of time is still a little beyond present day capabilities - but not for too much longer. If I had to throw a date into the ring, I'd suggest we should be looking for final settlement of the details of the mitochondrial free radical theory of aging no later than 2012.
That said, I suspect research teams will be entering clinical trials for therapies for the repair and replacement of damaged mitochondria en mass in the body somewhat in advance of that date. That feat has already been demonstrated in animals, and the pace of research is blistering these days.