They’re annoying and hard to get rid of once they invade the kitchen, but mice have long been a staple of medical research when trials are deemed too risky or uncertain for human subjects. (Indeed, they’re more common “guinea pigs” than actual guinea pigs.) And for a while, it made some sense: Mice and humans are both mammals and, to varying extents, pretty furry. But a new study involving nearly 40 researchers and a decade of data suggests our cheese-loving friends might make for lousy human proxies when it comes to predicting drug effectiveness. For the millions of lives dependent on mice-tested meds — not to mention the tens of billions spent on research — the implications could be enormous.
What’s the Deal
The study, published in the Proceedings of the National Academy of Sciences, compared the immune response of human patients with that of mice involving subjects with sepsis. A condition that The New York Times reports affects upwards of 700,000 Americans each year, sepsis occurs when the body’s immune system overreacts in fighting, among other things, potentially harmful bacteria or trauma from a burn. It can eventually prove fatal for between a quarter and half of victims.
What the researchers found was that the human body’s inflammatory response to trauma — specifically which genes are triggered in response — is very different than that shown in mice. In fact, a gene that was activated by trauma in mice was actually suppressed in the human body, which could make drugs effective in rodent trials catastrophic when used on humans. The study also raises concerns beyond sepsis, as conditions ranging from cancer to heart disease involve inflammatory immune responses that could very well operate differently across the two species.
Is It Legit?
Yes, however while these conclusions are making news worldwide, the concern isn’t all that new. Obvious physiological differences between mice and humans has limited research conclusions for decades (a discrepancy Greatist always tries to make clear when reporting new findings from the research front). What this study emphasizes is the dramatic difference between how mice and human immune systems operate, which could have a huge effect on the medical research industry moving forward. And while the results are likely to receive a lot of scrutiny and retesting over the coming years, they indicate that the clock is ticking on finding a suitable clinical replacement for Algernon.
Do you think mice make good proxies for human test subjects? Have and suggestions for alternatives? Let us know in the comments below or tweet the author @d_tao.