Yes, this is exactly the problem with animal models. We can tell that the animal has the same symptoms. We don't know that it has it through the same pathway as humans.
The models have worked often enough that it is reasonable to hope that what works in animals, will work in humans. And it is easier to experiment on animals. This is why they are used in research.
But when what works in animals doesn't work in humans, repeatedly, we should stop using that animal model in research.
Here are examples of treatments for Alzheimer's that worked in animals, reached human trials, then failed to help humans: AN1792 (active Aβ vaccine, Elan), Tarenflurbil (R-flurbiprofen), Semagacestat (γ-secretase inhibitor), Bapineuzumab (anti-Aβ mAb), Solanezumab (anti-Aβ mAb), Crenezumab, ponezumab, gantenerumab, and BACE inhibitors (e.g. verubecestat, atabecestat).
All of these were considered promising enough in mice to be worth expensive human trials. Where they failed. Those weren't cheap failures, either.
The models have worked often enough that it is reasonable to hope that what works in animals, will work in humans. And it is easier to experiment on animals. This is why they are used in research.
But when what works in animals doesn't work in humans, repeatedly, we should stop using that animal model in research.
Here are examples of treatments for Alzheimer's that worked in animals, reached human trials, then failed to help humans: AN1792 (active Aβ vaccine, Elan), Tarenflurbil (R-flurbiprofen), Semagacestat (γ-secretase inhibitor), Bapineuzumab (anti-Aβ mAb), Solanezumab (anti-Aβ mAb), Crenezumab, ponezumab, gantenerumab, and BACE inhibitors (e.g. verubecestat, atabecestat).
All of these were considered promising enough in mice to be worth expensive human trials. Where they failed. Those weren't cheap failures, either.