Why age? Should we end aging forever?

Why do we age and is there anything we can do about it?

In the US, people can expect to live to about 77 years old on average. Is this the best we can do? How much can we extend our lifespan? The oldest person on record lived to be 122 years old.

To answer these questions, we need to understand what happens to our bodies as we age. Are we programmed to live a certain number of years or do we wear out over time? These are two main theories of why we live as long as we do.

In the first, the idea is that our genes determine how long we live. We have a gene or some genes that tell our body how long it will live. If you could change that particular gene, we could live longer.

The second theory is that over time, our body and our DNA get damaged until we can no longer function properly. The idea here is that how long we last is really just a consequence of small changes in our DNA. These changes add up until the total amount of damage is too much to bear and we die.

It matters which theory is right, as it will determine how to push the limits of aging. For example, if how old we live is in our genes, then to increase our lifespan we may be able some day to change those genes. If on the other hand, our final age is based on the accumulated damage of a lifetime, then we could try to minimize that damage to live a longer life.

Which theory is right? Probably reality is a combination of these two ideas (plus some others we won’t discuss). In the past decade, scientists have found evidence to support both theories.

Work in animals, in particular in worms, has shown that mutating certain genes can increase lifespan about 4-fold. For humans, that would translate to about 300 years old! These results would seem to support that there are genes that determine how long we live.

Of course, if those genes are involved in fixing the damage that comes with aging, then the data would support the second model. In the well-known human disease called Werner’s syndrome, a mutated gene causes people to get older at a faster pace. The gene that is mutated is thought to be involved in DNA maintenance.

Other work shows that eating less increases how long animals will live. Although the reason for the increase in lifespan is unclear at this point, scientists have proposed that it has to do with decreasing DNA and cellular damage. Still other work suggests that cells can divide only a certain number of times. This is because of DNA at the end of chromosomes called telomeres that get shorter with each division. When they run out, the cell dies.

As you can see, trying to understand aging is a challenge. However, many scientists are fascinated by the questions of aging and the research is progressing fast. The following article is an example of the latest research on aging. The authors of the article use the mouse as a model to test the importance of mitochondrial DNA in aging.

What are mitochondria and are they making me old?

One popular scientific hypothesis proposes that mitochondrial DNA plays a major role in aging. What is mitochondrial DNA and why would it play an important role in aging?

Not all of our DNA is found in our nucleus. Some is actually found in small organelles within cells called mitochondria. Scientists think these mitochondria have their own pool of DNA because they were once small free-living creatures. Sometime in our distant past, our ancestors absorbed them and now mitochondria make our energy.

It turns out that mitochondrial DNA (mtDNA) gets mutations much faster than the DNA in the nucleus. One reason for this is thought to be the presence of ROS or “reactive oxygen species” (also known as “free radical”) in the mitochondria. When mitochondria make energy for us, they create ROS that can damage nearby mtDNA. In fact, this might be the reason why eating less leads to longer lives in animals — less food, fewer ROS.

The idea is that as mtDNA becomes more and more damaged, the mitochondria cannot produce energy as well and become dysfunctional. This could lead to aging and ultimately, death. Is there any way to test this idea directly?

The most direct way to test this hypothesis would be to increase the rate of DNA mutations and see if it results in an increased rate of aging. This is exactly the experiment done by a group of researchers in Sweden. The researchers mutated a gene in mice so that the mtDNA would get more mutations faster. (The way they did this was to modify the enzyme that copies mtDNA, DNA polymerase-g, so that it made more mistakes as it copied mtDNA. The end result of this is that over time, more mutations accumulate.)

As expected, the mutant mice had more mutations in their mtDNA. So did they age faster than normal mice? Yes. At about 25 weeks of age the mutant mice started to display signs of aging that are normally seen in much older mice. The mutant mice lived for less than a year instead of for 2 to 3 years.

So, obviously mutations in mtDNA are part of the aging process. Are they everything? Probably not but they are clearly an important part of the puzzle.

[Via: genetics.thetech.org]

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