Columbia researchers led by Lawrence S. Honig, MD, PhD, professor of clinical neurology in the Taub Institute, have found that telomere length influences the likelihood of developing dementia, as well as the remaining lifespan. Scientists have long been aware of a link between telomere length and cellular aging. The current research could lead to the use of telomere length as a marker of biological aging in people.
Telomeres, which some compare to the plastic tips on the ends of shoelaces, are small regions of DNA at the ends of the chromosomes that help protect the genetic information during cell division. When a cell divides, the two strands of DNA uncoil, and each strand is duplicated. But each time a cell divides, the telomeres get shorter. After 50–70 divisions, many cells show senescence, or signs of biological aging.
The researchers looked at telomere lengths in DNA samples from the white blood cells of 1,983 people age 66 to 101. They followed the subjects for an average of eight years and, after adjusting for age, education, and other factors, found that those with shorter telomeres had higher rates of dementia and mortality. As expected, older persons had shorter telomeres; in addition, men, on average, had shorter telomeres than women. This appears to be consistent with men’s being “biologically older.”
The chicken-and-egg question is: Do the shortened telomeres actually increase the risk of dementia and death? Or is some other factor both shortening the telomeres and increasing the likelihood of death? Finding a way to prevent telomeres from shortening could help to answer the question; it might also point toward a therapy, if shortened telomeres turn out to be causative of diseases of aging.
“Association of Shorter Leukocyte Telomere Repeat length With Dementia and Mortality” was published online in Archives of Neurology on July 23, 2012.
[Adaptation of digitally altered photo of telomere by Tryphon.]