Old before your time

Why do we grow old? It’s one of the most enduring mysteries in science, but now a team of European scientists have found a certain change in some people’s DNA that gives them a biological age much older than their age in years.

Image: Carlos Lorenzo/Flickr

We already knew that our risk of developing some age-related diseases depends more on ‘biological age’ than how long we’ve been alive, so this finding could help to identify people who are at high risk of developing some age-related diseases earlier in their life.

Growing old isn’t just a matter of how many years you’ve lived. True, that gives your chronological age, but the condition of the cells that form your body gives your biological age. In particular, the DNA is each of your cells has a cap on each end called a telomere, which get shorter every time the cell divides, so giving a clue to the cell’s biological age.

In the latest study, scientists have shown how people with a particular pattern in their DNA code have much shorter telomeres than other people, so their cells seem to be much older, biologically, than you would normally expect. In fact, the genetic change seems to add around 3.6 years to a person’s biological age!

This doesn’t mean that people with the variant are doomed to suffer from age-related diseases. Scientists still don’t understand exactly how gene variants can affect something as complicated as ageing, except that it may have some effect on how a near-by gene called TERC is switched on or off. Alternatively, it could make people more susceptible to other things that increase their biological age, such as smoking, obesity or lack of exercise.

It also takes us one step closer to understanding what this ageing thing is all about.

Paper Reference: Codd, V., et al (2010) Common variants near TERC are associated with mean telomere length. Nature Genetics, published online: 7 February 2010 doi:10.1038/ng.532

Born to drive (badly)

Could bad driving be blamed on our genes? Volunteers with a certain gene variant did much worse on a driving task than those without the variant, according to an American study. The result is rather surprising: our brains are tremendously complicated and the researchers didn’t think a single gene could have such a dramatic effect on behaviour.

"166 mph on the wrong side of the road, Officer? Sorry, it's my genes..." Image credit: Flickr/TrickyTM

The study suggests the gene in question helps people learn new physical tasks, such as driving along a complicated route, and remember how to complete the tasks in future. It works by producing a protein called BDNF, which helps neurons in the brain communicate with one another. Concentrating on something causes your brain to produce more BDNF in the brain region doing the thinking, letting it work more efficiently. People with the gene variant produce less BDNF so they don’t get this boost to brain power.

To test the variant’s effect on learning a complicated physical task, the researchers asked volunteers in a driving simulator to drive laps around a track. Those with the gene variant made more errors than volunteers without the gene variant. They also did badly when they repeated the task four days later.

So why have we evolved a gene variant that seems to make learning harder? It turns out the variant of BDNF does have one major advantage – people with it keep their mental abilities longer if they’re affected by diseases such as Parkinson’s, which damages brain function. Our brains, it seems, can be either very resilient to damage or very flexible when faced with learning and change, but not both.

Paper reference: doi:10.1093/cercor/bhp189

Of Mice and Men (and Mitochondria)

As people grow older, their bodies don’t function quite like they used to. New research suggests, however, that it is in fact a breakdown in how our bodies function that makes us grow old.

The researchers from the Karolinska Institutet in Sweden have discovered that badly-made proteins in mice cause them to age. As mice and humans are so genetically similar, the results could ultimately help us treat some human illnesses or even alter our own ageing process.

The proteins in question form part of the machinery that powers the mouse’s cells – the mitochondria. Mutations in the tiny bit of DNA inside the mitochondria mean that some of the proteins aren’t built correctly. These proteins quickly disintegrate, leaving the mitochondria short of vital components. Ultimately the cell is starved of energy and dies. We’ve known for a while that mutations in mitochondrial DNA have something to do with ageing, but the precise details of how this works have remained hidden, until now.

In people, faulty mitochondria can cause many diseases, but we know very little about how specific faults affect our cells. A better understanding of how our mitochondria and cells function will help to improve medical care: it may also help us find a way to slow or stop the ageing process entirely.

But with populations rising, and resources dwindling, could “curing” ageing be a double-edged sword?

Does this mouse want to live forever? Do you?

Image credit: Rama. Used under this licence.