Aging is at the root of some of the most important human diseases.

Figure: MODIFIED FROM F1000Prime Rep. 2013;5:5.

Figure: MODIFIED FROM F1000Prime Rep. 2013;5:5.

What if we could delay the many diseases of aging?

Aging is the single greatest risk factor for much of the disease in the developed world.

Aging leads to dramatic increases in rates of cancer, cardiovascular disease, and neurodegenerative disease (1–3). As the world’s population continues to age, the cost of these age-related diseases, in human suffering and in economic terms, will continue to increase (4).

Work to slow aging itself has the potential to simultaneously delay all of these diseases (5,6,7).

We can greatly alter aging in the lab. Our answers to the question of whether aging is alterable, and to what extent, have evolved very rapidly in recent years. Comparative studies have long pointed out hundred-fold variation in natural lifespan, even among otherwise very similar organisms (8). More recent work in lab-based genetic model organisms, including our own models, the budding yeast Saccharomyces cerevisiae and the nematode Caenorhabditis elegans, as well as the fruit fly Drosophila melanogaster and the mouse Mus spp, has demonstrated up to 10-fold changes in lifespan from mutations in a single gene (9–15). In many cases, mutations of the same gene greatly extended lifespan in invertebrate models and in mammals (16-19). This suggests that what we learn in the lab has a good chance of teaching us useful things about human biology.

Starting from genetic studies, this work has now progressed to identifying drugs that can remarkably extend lifespan in many organisms, including mice (20-23).

Interestingly, many of these genetic changes and drug treatments do not simply drag out the last part of life- rather, they appear to greatly extend the time during which organisms are healthy and youthful (i.e., their healthspan) (24-26).

Starting from findings in models like S. cerevisiae and C. elegans, some of these drugs are now moving into the testing phase in companion dogs (27, 28) and humans (29).

In the McCormick Lab, we are following several lines of ongoing research to uncover a more complete picture of the conserved genes that can affect aging in multiple organisms. We are using these results to build a deeper understanding of the underlying conserved biology of aging. We are also identifying drug targets and drugs that can delay aging in the lab in multiple organisms, in the hopes that these may also delay the onset of age-related diseases in humans.


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