Genomic responses in mouse models poorly mimic human inflammatory diseases

This is very important to us since inflammation is important in the neuronal cascade of death and in the formation of plaque. Ask your doctor to figure out what studies this may have compromised. My 164 hyperacute therapies would need some additional vetting based on this. And I bet a lot of the 1000 failures of rodent models may be explained by this.

 http://www.pnas.org/content/early/2013/02/07/1222878110

Abstract

A cornerstone of modern biomedical research is the use of mouse models to explore basic pathophysiological mechanisms, evaluate new therapeutic approaches, and make go or no-go decisions to carry new drug candidates forward into clinical trials. Systematic studies evaluating how well murine models mimic human inflammatory diseases are nonexistent. Here, we show that, although acute inflammatory stresses from different etiologies result in highly similar genomic responses in humans, the responses in corresponding mouse models correlate poorly with the human conditions and also, one another. Among genes changed significantly in humans, the murine orthologs are close to random in matching their human counterparts (e.g., R² between 0.0 and 0.1). In addition to improvements in the current animal model systems, our study supports higher priority for translational medical research to focus on the more complex human conditions rather than relying on mouse models to study human inflammatory diseases.

A blogger discussing it here:
Mouse Models of Inflammation Are Basically Worthless. Now We Know.