Experimental researches on animal models where the diseases are produced artificially are most popular form of research among scientists. This is however important to understand that a disease in human being may originate through a long process of mutually interacting physiological phenomenon creating a basis for the disease to erupt. A disease may be called acute on the basis of time taken to make it visible but its process is never acute as even an acute illness also has some malfunctioning ongoing for some time. In this case , when the path of generating a disease is different , how an animal experiment with a disease model can be beneficial to understand drug behavior in human diseases?
A very well known example of this problem is Alzheimer's disease models. With the exclusion of genetically modified models, most protocols create the disease in a mechanism totally different than the natural course in human.
But the problem isn't limited to pathogenesis. At the molecular level the situation could be really complicated. For example, drug target proteins could vary considerably across species in structure, interactions and subsequently in drug response.
That is why we should rely on collective results of previous studies and big data analysis rather than only one study or few.
I have the same doubts and questions, especially about extrapolating data from cell cultured to whole organisms.
But I guess the fact is--we don't have any better ways to approximate the answer
Thanks Ibrahim, Natalia and Navid for your interesting inputs. We do agree that experimental models may provide important clues about possible mechanistic details of action of a drug. The ultimate question however is if the process involved in production of disease equates to the process involved in diseases generation in humans. Take a small example of Diabetes mellitus in human which is a multi-factorial and complex disease in terms of its pathogenesis. Now can this pathogenesis of diabetes can be equated to a condition where diabetes is produced synthetically in a rodent by using some chemicals to kill the insulin producing cells?
Sanjeev Rastogi most definitely in case of diabetes and chemically injured beta cells the pathogenesis is way off. This model completely discounts the importance of adaptations that develop during the long prodromal stage. It only really allows to look at the endpoint pathogenesis.
I think we really need to look more into the populational studies to track changes in the human body that supersede the onset of the diseases. This would be much easier to achieve with proper health coverage, unfortunately given the current state of the healthcare in many countries, the people who tend to present with established diseases often times do not see their physicians on a regular bases so we are lacking medical history
Animal model can be chosen for primary safety and efficacy data. Really disease process is quite different from induced disease in model.
My limited understanding: Before animal model (in vivo) studies in vitro, and ex vivo data need to be considered. There are also ethical considerations. If an animal model is justified -- the choice of animal model needs to be justified. The knowledge gained in animal model studies is definitely not final...(they will provide general data that is relevant to humans due to important similarities with the animal model). Animal model studies will provide the basis for and justify clinical (human) studies.
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