This research has been doing the rounds:

This week researchers from the Dana-Farber Cancer Institute reported that the length of telomeres - which shorten with age - determines virtually every aspect of aging from wrinkles and gray hair to the onset of dementia, diabetes, and heart disease. At least that was the case in the mice they studied in a report published in Nature.

"We think we've identified the core pathway that really helps explain many different theories of aging," says study co-author Dr. Ronald DePinho, a geneticist at Dana-Farber. "Our study provides a unified field theory for aging."

In a nutshell, once telomeres shorten to a particular length, aging accelerates. Shortened telomeres allow the cell's DNA to become damaged, which activates a gene, p53. This sets off a warning to shut down the cells' normal growth and division cycle until the damage can be fixed or, if not, the cells die. At the same time, cells with short telomeres have power plants, or mitochondria, that are no longer operating at full capacity. This leads to malfunction in crucial organs like the brain, heart, liver, and pancreas, as well as a loss of muscle, and eventually extreme weakness and frailty.

(The paper is at Nature if you're the sort who likes to read primary sources). That's an ambitious declaration from the researcher quoted above - I can only imagine it's taken somewhat out of context and then hyped up by the science writer for the introductory paragraph, as it is certainly the case that damaged mitochondria and shortening telomeres are only two of the possible reasons we suffer age-related degeneration. Many of the other causes of aging involve a build up of varying forms of damaging waste product that the body cannot remove - mechanisms which are quite capable of causing disability and death on their own, telomere shortening or no telomere shortening.

That said, telomeres, mitochondria, and p53 are all large and healthy areas of research when it comes to the biology of aging. I imagine that anyone would be pleased to produce good evidence that might mechanically tie them all together, such that one or more are secondary effects rather than primary causes. From an economic perspective, we should all be hoping that some of our present candidates for the primary causes of aging turn out to be secondary effects - because then we don't have to devote any time towards developing repair biotechnologies to fix them.

On a closer reading of the new research, I have to say that it looks to me very much like an independent confirmation of discoveries from 2007 and 2008 relating to mitochondrial damage, telomere length, and the enzyme telomerase. In a nutshell, it may be that telomere shortening is entirely driven by mitochondrial dysfunction:

Researchers have put forward evidence to suggest that telomere shortening is caused by accumulated damage to mitochondrial DNA - essentially collapsing two areas of intense interest for gerontologists down to one root cause, if confirmed. ... [It may be the case that] poorly functioning mitochondria lead to telomere shortening, and telomerase somehow improves mitochondrial function to prevent that shortening. This is in place of the more expected path of undoing ongoing telomere shortening by adding extra repeat sequences to the end of the telomeres - that being the better understood function of telomerase.

I don't immediately see anything in the Nature paper that would rule out this interpretation of the link between these two fundamental mechanisms of aging. Like the earlier researchers, this present group also found that boosting telomerase activity improved mitochondrial function, though I believe they are arguing that the improved function happens as a secondary result of interactions between telomere length and p53. There's certainly plenty of room amidst the uncertainty for contradictory interpretations at this stage.

Time here looks at Ray Kurzweil's timeline for the development of biotechnologies that can defeat aging: repair the old, remove biological damage, and eliminate frailty and age-related death. "The Singularity isn't just an idea. it attracts people, and those people feel a bond with one another. Together they form a movement, a subculture; Kurzweil calls it a community. Once you decide to take the Singularity seriously, you will find that you have become part of a small but intense and globally distributed hive of like-minded thinkers known as Singularitarians. ... At the 2010 summit, which took place in August in San Francisco, there were not just computer scientists but also psychologists, neuroscientists, nanotechnologists, molecular biologists, a specialist in wearable computers, a professor of emergency medicine, an expert on cognition in gray parrots and the professional magician and debunker James 'the Amazing' Randi. ... After artificial intelligence, the most talked-about topic at the 2010 summit was life extension. Biological boundaries that most people think of as permanent and inevitable Singularitarians see as merely intractable but solvable problems. Death is one of them. Old age is an illness like any other, and what do you do with illnesses? You cure them. Like a lot of Singularitarian ideas, it sounds funny at first, but the closer you get to it, the less funny it seems. It's not just wishful thinking; there's actual science going on here. ... People have begun to realize that the view of aging being something immutable - rather like the heat death of the universe - is simply ridiculous. It's just childish. The human body is a machine that has a bunch of functions, and it accumulates various types of damage as a side effect of the normal function of the machine. Therefore in principal that damage can be repaired periodically. This is why we have vintage cars. It's really just a matter of paying attention. The whole of medicine consists of messing about with what looks pretty inevitable until you figure out how to make it not inevitable." I don't see it as plausible that we'll have everything in hand by 2045, but if we make a good start now, then we could have enough to put us into actuarial escape velocity - gaining life expectancy faster than we age, and thus able to wait for far better technologies that arrive later.

Link: http://www.time.com/time/printout/0,8816,2048138,00.html

The early posts at Chronosphere are well done and worth reading. The theme is a detailed and picture-strewn look at the history of cryonics, mixed in with considerations of our presently imperfect society and where it might be going next: "Chronosphere is your gateway to a fundamentally new way of living - in pursuit of physical immortality in a world of our own making - free from the tyranny of time, and the burden of injustice. Chronosphere will explore and create interfaces with the scientific, technological, social and moral resources needed to achieve these ends. Because we are all at risk of dying, cryonics will be a central focus of Chronosphere for the foreseeable future, but will be by no means be the only technology explored here. Interventive gerontology, with a strong emphasis on immediate, or very near term interventions to slow cognitive aging, will also be explored in detail. Join us on our quest to transcend the limits of time!"

Link: http://chronopause.com/

By virtue of the fact that very large sums of venture capital, big pharma investment, and public funding have been sunk into the examination of sirtuins in connection with longevity in mammals, I think we'll see a strong sirtuin research contingent in the scientific community for some years to come - and this regardless of the ultimate merits of this work. While there are promising signs that sirtuins may do something useful in terms of enhancing cellular housekeeping, after some years of research we have yet to see any of the promise of slowed aging that looked possible at the outset. See, for example:

• A Possible Reason For Sirtuin Uncertainty
• Critiquing the Sirtuin Model of Calorie Restriction

Research and development always takes longer than expected, but at this point I look at research into sirtuins as an early step forward on a much longer road - a part of the foundations of some later work, and producing little of direct use in and of itself. The newer technologies and newer companies who work on the same strategy of slowing aging via identification of ways to manipulate metabolism will leap over the work of the last five years, producing a hundred-fold more genetic and biochemical data in the process. Biotechnology is advancing so rapidly that each generation of development is made obsolete before it even hits its stride. It will be interesting indeed to see what comes after the present generation of biotech startups like Genescient and Halcyon Molecular.

But back to sirtuins: here is an optimistic open access paper from researchers who do see a bright future for the development of sirtuin-based therapies.

How does aging occur? Can we delay the aging process? These are questions that have been asked for hundreds if not thousands of years.

...

Aging is one of the most fundamental biological processes. It results in a decline in physiological function and an increased risk for pernicious diseases such as cancer. Oxidative stress has been proposed as a major cause of aging, but experimental tests of this hypothesis have been discouraging. Calorie restriction (CR) prevents age-related decline, but there are still gaps in our knowledge of the exact mechanisms underlying this feat. Finally, a tenuous balance exists between aging and cancer, calling for a search for interventions that prevent both aging and cancer. Recent work on the mammalian sirtuin SIRT3 has shed light on these long-standing issues and suggested new approaches to ameliorate the ravages of aging.

You might look back into the Fight Aging! archives for a quick overview of the relevance of SIRT3 to oxidative stress and longevity:

This research group proposes that Sirt3 acts on longevity through increasing antioxidants - we should all be appropriately skeptical, given the very mixed evidence for links between cellular antioxidants and longevity. That said, Sirt3 is located in the mitochondria, and the demonstrations of extended life spans through increased antioxidants have involved targeting those antioxidants to the mitochondria.

When considered in the broader context, a great many lines of research turn to point towards our mitochondria and the damage they suffer over time. All the more reason to direct greater efforts towards nascent mitochondrial repair technologies rather than yet more metabolic tinkering.

You might recall that the olm (Proteus anguinus) is a type of small salamander that lives as long as we do. Here researchers point out that olm life span is inconvenient for some theories of aging: "Recent work on a small European cave salamander (Proteus anguinus) has revealed that it has exceptional longevity, yet it appears to have unexceptional defences against oxidative damage. This paper comes at the end of a string of other studies that are calling into question the free-radical damage theory of ageing. This theory rose to prominence in the 1990s as the dominant theory for why we age and die. Despite substantial correlative evidence to support it, studies in the last five years have raised doubts over its importance. In particular, these include studies of mice with the major antioxidant genes knocked out (both singly and in combination), which show the expected elevation in oxidative damage but no impact on lifespan. Combined, these findings raise fundamental questions over whether the free-radical damage theory remains useful for understanding the ageing process, and variation in lifespan and life histories." Yet there are still the studies demonstrating extended life span through targeting antioxidants to mitochondria, which imply that at least so far as those cellular structures are concerned, oxidative damage is very important. It may be that the olm, like naked mole rats, has mitochondria that are highly resistant to damage in comparison to other species.

Link: http://www.ncbi.nlm.nih.gov/pubmed/21290398

A fair chunk of degenerative aging is caused by the accumulation of various kinds of damaging biochemicals, and here dry macular degeneration is added to that list: "A team of researchers, led by University of Kentucky ophthalmologist Dr. Jayakrishna Ambati, has discovered a molecular mechanism implicated in geographic atrophy, the major cause of untreatable blindness in the industrialized world. ... Concurrent with this discovery, Ambati's laboratory developed two promising therapies for the prevention of the condition. ... Geographic atrophy, a condition causing the death of cells in the retina, occurs in the later stages of the 'dry type' of macular degeneration, a disease affecting some 10 million older Americans and causing blindness in over 1 million. There is currently no effective treatment for geographic atrophy, as its cause is unknown. Ambati's team discovered that an accumulation of a toxic type of RNA, called Alu RNA, causes retinal cells to die in patients with geographic atrophy. In a healthy eye, a 'Dicer' enzyme degrades the Alu RNA particles. ... We discovered that in patients with geographic atrophy, there is a dramatic reduction of the Dicer enzyme in the retina. When the levels of Dicer decline, the control system is short-circuited and too much Alu RNA accumulates. This leads to death of the retina. ... Alu elements make up a surprisingly large portion - about 11 percent by weight - of the human genome, comprising more than 1 million sequences. However, their function has been unknown, so they have been called 'junk' DNA or part of the 'dark' genome. The discovery of Alu's toxicity and its control by Dicer should prove of great interest to other researchers in the biological sciences ... Ambati's team developed two potential therapies aimed at preventing geographic atrophy and demonstrated the efficacy of both approaches using laboratory models. The first involves increasing Dicer levels in the retina by 'over-expressing' the enzyme. The second involves blocking Alu RNA using an 'anti-sense' drug that binds and degrades this toxic substance. ... Ambati's group is preparing to start clinical trials by the end of this year."

Link: http://www.eurekalert.org/pub_releases/2011-02/uok-pdi020311.php