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A biogerontologist at work

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As promised, I will attempt to explain my work in a way that will allow everyone to both understand and appreciate it.

To most people I am a scientist, which is of course true. I will leave the discussion of what makes a scientist for another post (though it’s certainly worth an inquiry), and for now leave it at “someone who finds things out”. So, I find things out. About what? To the scientific community, I would be considered a biogerontologist. Gerontology is the study of aging (literally the “study of an old man), and the bio- prefix implies that I focus on the processes that occur in our bodies as we age, rather than say the social impact of an aging population.

So, what happens as we age? The truth is, we don’t really know. We can all see the symptoms: wrinkled skin, brittle bones, failing memory, grey hair, weakness, disease, death. For each symptom, we look for solutions. Pills to lower blood pressure, canes to help us walk. The problem is, of course, that treating the symptoms won’t cure the ailment. A doctor can know the symptoms, and the best way to mitigate them, but without knowing their cause he can do no more than to slow the process. The role of the biogerontologist is to uncover the root of the problem, to illuminate the biological processes that lead to this deterioration.

We all grow older, and weaker...

There are, however, theories. I imagine that most of the people reading this will know about DNA; long strands of genetic code, containing every shred of information about our bodies. A copy of this genetic encyclopedia is stored in the core of most of the cells that make up our bodies, and is constantly consulted by the cell when making proteins. Proteins (aside from being found in meat) play numerous roles inside each cell, from long strings holding things together, to tiny walkers moving cellular components around. Basically, proteins take care of mostly everything that happens in the bodies, so obviously their functioning correctly is pretty important. And as I said, because DNA serves as their blueprint, any errors in the DNA will translate to errors in the proteins. Which finally brings me to my point, being that one theory of aging is that accumulating damage to our DNA causes our bodies to gradually perform worse and worse, and eventually fail. Which is of course exactly what happens with aging. So intuitively it makes sense, and there’s a lot of evidence to suggest that it plays some role at least.

Now, DNA can be damaged in many different ways. Many of us have heard recently that getting too much sun can give you skin cancer because of the UV radiation; well, that’s one type of DNA damage. Then there’s nasty chemicals (from things like cigarettes, pesticides, fungus and more) getting into our cells and messing up the DNA.  And oftentimes, the cell simply messes up when translating the DNA into proteins, or when it’s copying the DNA in preparation for cell division. All in all, damage to our DNA happens a dozen times every second, and if nothing was done about this damage, we’d probably all die from cancer or simple system failure while still in our teens. The fact that we don’t provides the most obvious proof that our bodies have a wide variety of (protein) tools to fix DNA damage as it occurs, and in fact manages to repair almost, but not quite, all the damage that occurs. Our DNA damage theory of aging suggests that this remaining damage is what causes all the debilitations that come with age, and the first question that springs to mind is how we can avoid that damage.

That’s the fundamental question we operate around at the Laboratory of Molecular Gerontology, though it’s not often spoken out loud. Our work consists mainly of investigating the proteins involved in DNA repair, finding out how and when they work, when and why they don’t work, how they work together, what makes them tick. This research takes a number of forms in terms of actual work in the lab, of which I’ll present just a couple of examples in simple terms:

  • Co-Immun0precipitation – The objective here is to determine what partners a given protein has contact with in the cell. It works like this: You take a number of human cells and add a liquid that makes them burst. Now you’ve got all the innards from the cells, and want to pick out your protein of choice. So you add an antibody tailored by some poor rabbit’s immune system to recognize and bind to exactly that protein, which it proceeds to do. Now you’ve got your protein with antibody bound, so you can add some relatively big beads that the antibody is known to stick to (which it proceeds to do) and then filter the beads out of the cellular soup. So then you have your protein stuck to the beads via the antibody, as well as anything that stuck to your protein when you started the process, and it’s a simple matter to boil the protein off the beads and then look at what else you caught in the process.
  • Helicase assays – Now we want to test whether a given protein is able to separate paired DNA strands, an activity that’s often involved in DNA repair (and termed helicase activity). This is pretty simple really. What you do is to mix up some of your protein with some paired DNA, with a marker on one of the two strands, and let the hypothetical helicase work its magic for a while (or not). Then you stop the reaction and stick everything into a gel, which is basically a big mess of tangled cables, and force the DNA to go through the gel. It’s harder to force something big through a tangled mess than it is something small, so any strands that were separated will travel further through the gel in a given time frame than a pair of strands stuck together would. So, if you look at how much marker traveled further (if any) compared to the amount that traveled more slowly, you can see whether your protein works as a helicase, and how well.

Doing things like these, we slowly begin to understand the workings of our DNA repair machinery. On the surface, this merely serves to sate the appetite of those inherently curious personalities we call scientists, but the (realistic) hope is of course that understanding the machinery will allow us to intervene and make improvements, as humans are wont to do to anything we interact with. Maybe, at some point in the future, growing older won’t necessarily mean growing weaker; imagine if we could just keep doing anything we wanted to, as long as we felt like it. That’d be pretty cool.

...but do we have to?


Written by Martin

2010/05/25 at 21:31

Posted in Uncategorized

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