"All diseases run into one, old age" -Ralph Waldo Emerson

Humanity is facing a challenge with profound implications in all aspects of life. If you pay attention to the media you're probably thinking climate change or the worldwide economic crises are paramount, but there is another issue which, in my humble opinion, trumps them all yet receives little to no recognition; aging.

As standards of living rise in developing nations and healthcare interventions continually improve the quality and duration of life, limited natural resources and rising prices of those aforementioned life-extending technologies will rear their ugly heads. Another phenomenon to take heed of is population aging. People are not just living longer, but the number and proportion of the elderly population is getting larger. The per-capita cost of maintaining health in the elderly is significantly more than for a younger person, and like a see-saw with a fat kid on one end and a little runt on the other, the costs of maintaining social health programs (like medicare and medicaid in the US) will far outweigh the funds and subsidies provided by tax revenue from the younger, working class.

With that in mind, I think basic research on the molecular properties of aging are vital for discovering potential 'fountains-of-youth' - interventions for extending healthy life span, key word being healthy and implying drastic reductions in cost. At the cellular level, one characteristic of aging being studied is dysfunction in the maintenance of proper-functioning DNA. The human body is composed of trillions of human cells (and even more bacterial cells) which maintain functionality throughout life by replicating DNA and forming new cells (just like periodic oil changes keep a car running smoothly). This process, called mitosis, is tightly controlled by cells and is susceptible to age-associated malfunctions leading to genomic instability and tumorigenesis (normal cells becoming cancerous). Research at the Mayo Clinic identified a gene involved in the mitotic pathway - BubR1 - whose decreased expression (remember DNA -> RNA -> Protein from basic Biology? Decreased expression is less DNA -> RNA) in mice is associated with age-related dysfunction in multiple organs "including heart, muscle, kidney and eye". More importantly, increasing the expression of BubR1 (more DNA -> RNA) prevented these issues and the mice were healthier for longer. So what? What's the big deal with helping mice live longer? Well, human DNA also contains the BubR1 gene and if a decreased expression can be associated with aging, voila.

While this discovery may not be the 'straw that breaks the camel's back' for healthy aging research, it does contribute to our understanding of the complex process (and problem) that is aging. And maybe, just maybe, with a bit of luck and a lot of determination, could someday help us turn back the clock and raise that overweight see-saw'er off the ground.