Are some mouse models better than others?

Do Mice Make Bad Models? A study suggests that some mouse models do not accurately mimic human molecular mechanisms of inflammatory response, but other mouse strains may fare better. By Dan Cossins | February 11, 2013
Excerpt: “There needs to be a higher degree to which a model reproduces human disease in terms of molecular mechanisms, rather than just phenotype.”
My comment: Re: “There needs to be a higher degree to which a model reproduces human disease in terms of molecular mechanisms, rather than just phenotype.”
First, I will reiterate: The molecular mechanisms of adaptive evolution and disease are the same despite phenotype. They are nutrient-dependent and pheromone-controlled in species from microbes to man. This is best exemplified in the honeybee model organism — an animal model readily extended to mammals. For example, the immune system and olfactory system of invertebrates (e.g., the honeybee) and mammals distinguish genetically predisposed self from non-self differences. The differences enable natural selection for the most beneficial non-self nutrients and social selection that precedes sexual selection for genetic diversity.
In stark contrast to these biological facts (above), there is a theory that mutations somehow cause evolution. That theory places the epigenetic effects of nutrient stress and social stress on the microRNA / messenger RNA balance and alternative splicings outside the context of what is now known about the molecular mechanisms involved in health and disease accross an evolutionary continuum.
It is long past time that students are taught the biological facts about animal models and adaptive evolution. The tweaking of immense gene networks in superorganisms —  like the honeybee — that solve problems through the exchange and the selective cancellation and modification of signals is caused by the epigenetic effects of nutrients and pheromones on genetically predisposed ecological, social, neurogenic, and socio-cognitive niche construction that link gene expression to behavior and back.
Clearly, an environmental drive evolved from nutrient uptake in unicellular organisms like yeasts to nutrient intake and socialization in insects via the same molecular mechanisms that link food odors and pheromones to changes in hormone-organized and hormone-activated changes in mammalian behavior, including hormone-driven changes in human behavior. This clarity of my model of adaptive evolution is obviously consistent with what’s known about molecular biology when viewed in the context of olfaction and odor receptors, which provide a clear evolutionary trail that can be followed from unicellular organisms to insects to humans.
Lack of clarity and inconsistent results from different model organisms, including mouse models that have been “created” in the lab, attests to missing information about the basic principles of biology and levels of biological organization that enable nutrient-dependent pheromone-controlled adaptive evolution. In some cases, a theory of mutation-caused evolution has been substituted, which appears to make some people think that their derived theories can be compared to a model of nutrient-dependent pheromone controlled adaptive evolution. Their comparisons end when their theory-derived mouse models fail to reproduce human disease in terms of molecular mechanisms of nutrient-dependent epigenesis and pheromone-controlled epistasis.
 
 

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