I’m kinda new to this - so what you’re saying is the mouse model induces beta-amyliods directly, rather than finding ways to give mice Alzheimer’s, whereas the human tests are for humans that have Alzheimer’s? Meaning we aren’t doing any tests of simply stimulating BA growth in humans?
I'm also not exactly on expert on this myself, take it with a grain of salt, but my understanding is that we don't really know what Alzheimer's is. To our knowledge there isn't a clear physical cause we can point to - a virus or bacteria or tumor or something. We have the symptoms, and we have the observation that Alzheimer's patients have amyloid plaques in their brain - among other differences!
Since mice don't ever get Alzheimer's naturally, and we don't actually know what Alzheimer's is, we don't know what it would even mean to give mice Alzheimer's. But for research we've genetically engineered mice that end up with lots of those plaques, and their behaviour does suggest an impairment similar to Alzheimer's, so that's what we've been working with. And in those models, various treatments that involve clearing the plaques does seem to help resolve that impairment - but they don't help humans with Alzheimer's, even if they do clear the plaques there too.
If I'm reading your question correctly, we can't stimulate amyloid plaque growth in humans for experimentation because that'd almost certainly be considered completely unethical. And also our methods for inducing the amyloid plaques involve mice that are genetically modified from birth rather than something we introduce in vivo, which would somehow be even more unethical than experimenting on live humans. It's possible we could make those genetic modifications in vivo now with recent developments in gene therapy, but...why?