Gordon J. Lithgow

Gordon J. Lithgow (born 25 March 1963 in Motherwell, Scotland) is a Scottish medical researcher.

Lithgow grew up in Newarthill in North Lanarkshire, traditionally a mining village, and attended Newarthill Primary School and Braidhurst High School, Motherwell. He graduated from the University of Strathclyde in 1985 with a degree in Applied Microbiology and then started work towards a PhD in the laboratory of Alistair Brown at the Institute of Genetics at the University of Glasgow. He defended his PhD thesis in 1989 on transcription mechanisms in yeast. He then moved to Basel, Switzerland, to further study yeast molecular biology. There he became interested in the possibilities of studying aging in simple laboratory animals. This prompted a move to the University of Colorado, Institute for Behavioral Genetics, and to the laboratory of Thomas E. Johnson who was studying the first genetic mutation to slow aging in a gene he called age-1.[1]

After making a series of discoveries linking aging to stress,[2] Lithgow established his own independent laboratory at the University of Manchester, England which investigated the relationship between stress and aging. He moved the lab in 2001 to the newly established Buck Institute for Research on Aging.[3]

Throughout his career, Lithgow was a prominent spokesperson for aging research and frequently interacting with print, radio and television media. He has appeared on the Today program on Radio 4[4] and has given interviews to numerous national newspapers, including the New York Times[5] and The Guardian about aging and his research, and has presented to science-loving lay audiences.[6] He gave an extended interview about aging science to The Science Network.[7]

Lithgow sheds light on the mechanisms of aging by identifying agents that extend lifespan or prevent age-related disease. He has discovered a range of factors that can lengthen life in the microscopic worm Caenorhabditis elegans, and he applies these findings to studies in human cells in culture. Much evidence points to stress contributing to a breakdown in the ability to maintain optimal molecular stability resulting in aging and disease. Certain life-extending agents help C. elegans respond to lifelong stress by remodeling the natural stress fighting cellular mechanisms, the Lithgow lab has found. For example, long-lived mutants of C. elegans can are very stress resistant as a result of elevated levels of “heat shock proteins”. Heat shock proteins promote longevity probably by preventing a loss of protein balance. Long-lived mutant strains are also resistant to heavy metals, so the Lithgow lab went on to study the relationship between longevity and “metallostasis.” [8]

The Lithgow lab has discovered that certain cell proteins capable of extending life can also be closely involved in disease prevention. But when proteins play such dual roles, they may sometimes make tradeoffs that affect the fate of the organism. Lithgow is studying genetic variations in “checkpoint proteins’’ that may create a trade-off between the rate of aging and incidence of cancer.[9]

The Lithgow lab has made seminal discoveries in the use of pharmacological agents to intervene in aging processes, such as antioxidants that protect cells against damage from unstable chemicals called free radicals. More recently, his lab have uncovered compounds that act as “stress response mimetics” that maintain protein balance and stability. These compounds suppress pathology associated with Alzheimer’s disease.[10] The lab continues to undertake screens for chemical compounds that slow aging and extend healthspan.

He is the principal investigator and director of the Buck Institute’s Interdisciplinary Research Consortium on Geroscience.[11] He is also the principal investigator of the Larry L. Hillblom Network on the Chemical Biology of Aging, and is the coordinator of the Hillblom Center for the Biology of Aging Support Award.[12]

References

  1. ↑ Johnson TE, Lithgow GJ. The search for the genetic basis of aging: the identification of gerontogenes in the nematode Caenorhabditis elegans. J Am Geriatr Soc. 1992 Sep;40(9):936-45.
  2. ↑ Lithgow GJ, White TM, Melov S, Johnson TE. Thermotolerance and extended life-span conferred by single-gene mutations and induced by thermal stress. Proc Natl Acad Sci U S A. 1995 Aug 1;92(16):7540-4.
  3. ↑ Dodge V, Melov S. The Buck Institute for age research. Exp Gerontol. 2001 Feb;36(2):205-8.
  4. ↑ http://news.bbc.co.uk/2/hi/science/nature/904722.stm
  5. ↑ http://www.nytimes.com/2011/04/05/science/05obworm.html?_r=0
  6. ↑ "Gordon Lithgow at Health Extension Salon #7". http://HealthExtension.co''. Health Extension. 2013-03-28. Retrieved 26 June 2013.
  7. ↑ http://www.youtube.com/watch?v=LM4oe3nV5SY
  8. ↑ Page KE, White KN, McCrohan CR, Killilea DW, Lithgow GJ. Aluminium exposure disrupts elemental homeostasis in Caenorhabditis elegans. Metallomics. 2012 May;4(5):512-22. doi: 10.1039/c2mt00146b. Epub 2012 Apr 26.
  9. ↑ Olsen A, Vantipalli MC, Lithgow GJ. Checkpoint proteins control survival of the postmitotic cells in Caenorhabditis elegans. Science. 2006 Jun 2;312(5778):1381-5.
  10. ↑ Alavez S, Vantipalli MC, Zucker DJ, Klang IM, Lithgow GJ. Amyloid-binding compounds maintain protein homeostasis during ageing and extend lifespan. Nature. 2011 Apr 14;472(7342):226-9. doi: 10.1038/nature09873. Epub 2011 Mar 30.
  11. ↑ http://geroscienceonline.org/
  12. ↑ http://www.buckinstitute.org/Hillblom_Center