Our time is limited. The clock is ticking. If we’re fortunate enough to escape disease, accidents, or war intact, then at some point our bodies eventually turn against us. What causes our bodies to age? Why don’t we simply live on (until that proverbial anvil lands atop our unsuspecting heads)?

Turns out, telomeres are one piece of the aging puzzle. They act like tiny timers – and once they run out, well, so do we. Chromosomes constantly replicate themselves through cell division, and telomeres are the protective end-parts of chromosomes. When chromosomes are copied, however, these telomeres shorten a little bit with each round of cell division.

The good news? This shortening is kept in check by the enzyme telomerase which elongates the telomeres. (Whew.)

The bad news? We have a limited supply of telomerase. (D’oh!)

What happens when our bodies cannot effectively elongate telomeres? The short answer is, we begin to age. People who cannot effectively elongate telomeres at a relatively youthful age may develop age-related diseases such as bone marrow failure, immune senescence and pulmonary fibrosis. This is known as Telomere Syndrome.

Carol Greider, 2009 Nobel Laureate and professor at Johns Hopkins University, discusses how this seemingly benign structure on the end of a chromosome – the telomere – can affect human disease and aging.

Watch this informative video to learn more: How can telomeres cause age-related disease?, part of the UC Berkeley Graduate Council Lecture series.