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McCormick Lab

Principal Investigator: Mark McCormick

Assistant Professor, Department of Biochemistry and Molecular Biology

Laboratory Photo

Contact the Laboratory

Lab Physical Address

Biomedical Research Facility, Room G20

Lab Mailing Address

McCormick Lab
MSC08 4670
1 University of New Mexico
Albuquerque, NM 87131-0001

Phone: (505) 272-7564

Research Interests

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.  We hope that these may also delay the onset of age-related diseases in humans.

We are increasingly focusing on what is now being called data science, applying programming in R / Python / etc. to implement techniques from basic statistics to machine learning, in order to speed our work to understand aging.  Prospective lab members with strengths or interests in these areas are encouraged to contact us.


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  2. Butler, R. N. et al. New model of health promotion and disease prevention for the 21st century. BMJ 337, a399 (2008).
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  10. Kenyon, C., Chang, J., Gensch, E., Rudner, A. & Tabtiang, R. A C. elegans mutant that lives twice as long as wild type. Nature 366, 461–4 (1993).
  11. Kennedy, B. K., Austriaco, N. R., Jr., Zhang, J. & Guarente, L. Mutation in the silencing gene SIR4 can delay aging in S. cerevisiae. Cell 80, 485–96 (1995).
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  15. McCormick, M. A. et al. A Comprehensive Analysis of Replicative Lifespan in 4,698 Single-Gene Deletion Strains Uncovers Conserved Mechanisms of Aging. Cell Metab. 22, 895–906 (2015).
  16. Blüher, M., Kahn, B. B. & Kahn, C. R. Extended longevity in mice lacking the insulin receptor in adipose tissue. Science 299, 572–574 (2003).
  17. Holzenberger, M. et al. IGF-1 receptor regulates lifespan and resistance to oxidative stress in mice. Nature 421, 182–187 (2003).
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  20. Harrison, D. E. et al. Rapamycin fed late in life extends lifespan in genetically heterogeneous mice. Nature 460, 392–395 (2009).
  21. Miller, R. A. et al. Rapamycin, but not resveratrol or simvastatin, extends life span of genetically heterogeneous mice. J. Gerontol. A. Biol. Sci. Med. Sci. 66, 191–201 (2011).
  22. Harrison, D. E. et al. Acarbose, 17-α-estradiol, and nordihydroguaiaretic acid extend mouse lifespan preferentially in males. Aging Cell 13, 273–282 (2014).
  23. Bitto, A. et al. Transient rapamycin treatment can increase lifespan and healthspan in middle-aged mice. eLife 5, (2016).
  24. Garigan, D. et al. Genetic analysis of tissue aging in Caenorhabditis elegans: a role for heat-shock factor and bacterial proliferation. Genetics 161, 1101–12 (2002).
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  28. Urfer, S. R. et al. A randomized controlled trial to establish effects of short-term rapamycin treatment in 24 middle-aged companion dogs. GeroScience (2017).
  29. Mannick, J. B. et al. mTOR inhibition improves immune function in the elderly. Sci. Transl. Med. 6, 268ra179 (2014).