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If You Give a Mouse a Drug…

February 17, 2013

Evolution is a fascinating thing. It is what connects each of us to one another, to our ancestors, and to each creature around us. Recent research has allowed genetic similarities to be distinguished between individuals of different species; these similarities have proven human relations to chimpanzees along with many other fascinating discoveries. How far after species evolve from a common ancestor do they stop being accurate models for disease in one another?
Long before evolution was being studied on a genetic scale, however, humans had determined certain model species which worked as preliminary test subjects for drugs and treatments that would later be used on humans. It was thought that mice were a very useful model for humans, and in some cases they still are. However, recent genetic studies have been performed that prove that mice may not be the best test subject for sepsis, burns, and trauma, three major human killers.
A study by Junhee Seok et. al was published on January 7, 2013 in PNAS on the differences between mice and human reactions to the aforementioned ailments. I heard of this article in my population genetics class and when I researched it I found a synopsis of it posted in New York Times Science on February 11, 2013, both articles are linked below. The researchers looked at expressed genes in white blood cells of sick patients both of mice and of humans. Their results were shocking. They found that many mice react in a way that is exactly opposite of the genetic reactions of humans, expression of genes in mice may be suppression in humans. These differences mean that drugs developed for curing mouse patients could potentially be harmful for human patients. Over 150 drugs in the past have been successful for trials in mice and unsuccessful in humans. This paper suggests that the reason of these drug failures could be that mice are not ideal model species. Other evidence contributing supporting this theory is that mice must be infected with a million times more bacteria to show symptoms than what would kill humans.

This brings me to the question of how far along in evolution do two species differ so far from one another that they are no longer models of one another? While I don’t believe this question has been answered, it fascinates me. I wonder if isolated populations of the same species, after being subjected to natural selection, would react differently to infection. Perhaps speciation is the limit of host modeling, but after a speciation event they no longer react the same. Or maybe there is a certain point neither speciation or population isolation that separates one model from another. If this is the case I’d be curious to see if the amount of evolutionary time was the same between each model. Maybe after this mouse study other researchers will look at genetic differences in other model organisms and get closer to answering my questions. I certainly hope so!

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