Telomere stress reveals insight into ageing

March 1, 2012
Telomere stress reveals insight into ageing

Scientists at Newcastle University have unlocked clues that give us a greater understanding of the ageing process. 

In research published in the journal , the team, led by Dr. João Passos, has shown that stress-induced damage to the ends of our chromosomes may be an important factor.

in our bodies divide to replace cells that are worn out or damaged. During this division, copies of our genetic material are passed on to the next generation of cells. The genetic information inside cells is arranged in twisted strands of DNA called chromosomes and at the end of these strands is a protective 'cap'. Previous research has shown that telomeres get shorter each time a cell divides. This shortening has been linked to the aging process because cells are no longer able to divide past a critical minimum telomere length.

While current thinking on how telomeres affect ageing has focused mainly on telomere length, this new research highlights that there is considerably more to the story.

Dr. João Passos said: "As we age, telomeres do indeed get shorter, and premature shortening of telomeres heightens the risk of diseases and death. However, our findings show that telomeres in both humans and mice are particularly susceptible to DNA damage and that stress-induced damage to telomeres, even long ones, is irreparable and increases with age."

As we grow old, cells progressively accumulate damage to DNA - the molecule containing the genetic information that is necessary for the development and functioning of all living organisms. However, this damage - which is mostly caused by free radicals - can be fixed by the cells repair machinery.

The research is the outcome of Dr. Passos’ Biotechnology and Biological Sciences Research Council (BBSRC) funded David Phillips Fellowship.

The Newcastle University discovery shows that ends of chromosomes are particularly sensitive to stress and are not so efficiently repaired. Damage within telomeric regions remains unrepaired and this helps to explain why cells lose their ability to regenerate as they age.

"This discovery improves our understanding of how telomeres impact on cellular ageing. We now know that telomeres are unusual in the way they respond to damage and that it is not only their length that counts as our cells age", said Dr. Passos. "Future research will need to focus on unravelling the properties which make these regions of the genome so special, so that we can devise therapies to improve telomere repair." 

Explore further: Ultra short telomeres linked to osteoarthritis

Related Stories

Ultra short telomeres linked to osteoarthritis

January 16, 2012

Telomeres, the very ends of chromosomes, become shorter as we age. When a cell divides it first duplicates its DNA and, because the DNA replication machinery fails to get all the way to the end, with each successive cell ...

Recommended for you

Functional human liver cells grown in the lab

November 26, 2015

In new research appearing in the prestigious journal Nature Biotechnology, an international research team led by The Hebrew University of Jerusalem describes a new technique for growing human hepatocytes in the laboratory. ...


Adjust slider to filter visible comments by rank

Display comments: newest first

not rated yet Mar 01, 2012
What is the stress factor being allured to? Is it physical, mental or even perhaps cellular? The reason I ask, if it is physical such as in exercise, then that would be a significant impact on exertion of the human body. To me, I find this impractical since the very act of resistance training does build muscle. Curious on the thoughts of others on the subject. We all would like to live longer
not rated yet Mar 04, 2012

Note the commentary thread. An astute reader highlights the immortality of human stem cells.

Please sign in to add a comment. Registration is free, and takes less than a minute. Read more

Click here to reset your password.
Sign in to get notified via email when new comments are made.