In pre-clinical trials for some diseases, animal models are notoriously nearly useless. The story of the C9orf72 mice model (a familial ALS/MND model) who lived healthily in a Broad lab, while their counterparts at Harvard died quickly [0, 1] has been widely discussed.
In general, for nervous system diseases, mice models are not translatable to humans. One reason might be that their nervous system is quite different from those of primates/humans, for example, great primates have direct motor neuron connections (no interneurons) for complex manipulations.
So scientists often try to develop animal models closer to primates, see for example [1]. But their methodology for validating animal models intrigues me.
Basically, they seek to disrupt to some extent some biological function, and if the behavior/phenotype of the animal model looks like that of human patients, then it is assumed the animal model is correct.
I wonder if it's not possible to use a software model of a human being with the same level of effectiveness. For example, there are very complex software models of human beings (see Biogears engine and similar [3]).
If we apply the same methodology to human software models and if when we disrupt a biological function, and if then the software model displays the pathological behavior, isn't as valid as an animal model?
I would be interested to know your advice.
[0] https://www.alzforum.org/news/research-news/gut-microbes-dif...
[1] https://pubmed.ncbi.nlm.nih.gov/32483373/
[2] https://pubmed.ncbi.nlm.nih.gov/39343009/
[3] https://www.biogearsengine.com