I was sent an article in the lay press which was followed by the scientific article referenced within the lay article for the “Beyond the Medical Headlines” weekly column that I do for our health system. The article in the lay press had an intriguing title involving “Zombie cells.” The scientific article was a little more subdued (Clearance of p16[Ink4a]-positive senescent cells delays aging associated disorders) and can be found in the journal Nature. The zombie fixated lay writer started with a fairly circumspect quote from on of the investigators:

“By attacking these cells and what they produce, one day we may be able to break the link between aging mechanisms and predisposition to diseases like heart disease, stroke, cancers and dementia,”

but finished it off with a quote that was a little over the top:

“There is potential for a fundamental change in the way we provide treatment for chronic diseases in older people.”

I would be the first to agree that there is potential for fundamental change in healthcare…I have trouble believing that rat doctors will lead the charge in the immediate future

The study was done with mice that are genetically altered to become old quicker than normal rats (who get old pretty quick anyway). They then used a proposed marker for cell aging (p16[Ink4a) and developed a method of removing these “old” cells. The mice were compared to untreated mice at 10 months. The treated mice looked much more ready for a close-up and ran faster on the treadmill than the untreated mice. It is a long way from 10 month old rats to 70 year old people who have smoked for 60 of those years, spent a total of 30 years in the sun, have a sedentary lifestyle and are double the weight that they should be.

If you are interested in how the rats live prior to their untimely demise in the name of research, here is a good article. Here is someone else’s take on translating rat medicine to humans. The bottom line:

The current approach to studying arrhythmia and many other diseases goes back to a three-step protocol worked out by the German scientist Rudolf Virchow, Efimov says. The first step is to identify the clinical signs and symptoms of the disease; the second is to recreate those symptoms and identify a therapy in an animal model; and the third evaluate the safety and efficacy of the therapy in clinical trials. “The problem is that at least in the cardiac arrhythmia field, this paradigm has had very few successes,” Efimov says. “It has resulted in the discovery of almost no successful drugs. Clinical trial after clinical trial has ended in failure.” Mice are the most popular animal model in physiology, but the mouse is not a very good model for cardiac physiology. “A mouse’s heart beats about 600 times per minute, so you can imagine it is a little different from humans, whose hearts beat on average 72 times per minute,” Efimov says. “You can mutate in mice the gene thought to cause heart failure in humans and you don’t get the same disease, because the mouse is so different,” Efimov says. “So, unfortunately, even with the help of transgenic mice, very few results made it from the animal model to the clinic.” The answer, Efimov says, is to insert an additional step in the three-step research protocol. After a therapy has been tested in an animal model, it should be tested in human hearts before moving to clinical trials. “Since we’ve begun to work with human hearts,” he says, “we’re finally starting to catch up with animal physiology.”