Biology is always more complex than first appears. I noticed a good example a few days ago, and have been mulling over what to say about it. You may have noticed that research into the biochemistry of progerias - accelerated aging conditions - has been picking up in recent years. The same is true of research into the mechanisms of calorie restriction, such as the importance of enhanced autophagy to health benefits conferred by the practice of calorie restriction. Progress has been made on both fronts, with the possibility of beneficial medical advances in longevity science resulting in the future. Much remains to be understood, however.

Here's a complication thrown into the picture built to date:

It is widely-assumed that the autophagic activity of living cells decreases with age and probably contributes to the accumulation of damaged macromolecules and organelles during aging. Over the last few years, the study of segmental progeroid syndromes in which certain aspects of aging are manifested precociously or in exacerbated form, has increased our knowledge of the molecular basis of aging. We have recently reported the unexpected finding that distinct progeroid murine models exhibit an extensive basal activation of autophagy instead of the characteristic decline in this process occurring during normal aging.

Further studies on Zmpste24-null progeroid mice, which are a reliable model of human Hutchinson-Gilford progeria, have revealed that the observed autophagic increase is associated with a series of metabolic alterations resembling those occurring under calorie restriction or in other situations reported to prolong lifespan.

So, what does this mean? That we've reached the point in the capabilities of biotechnology at which there is little more to be learned about "normal" aging from progerias? That progeroid mice eat less? That the stress effects of progeria upon cells trigger the same sort of response as the stress of calorie restriction?

Of such challenging questions is fundamental research made.