It’s pretty clear that the commenter you’re responding to is making the point that a treatment effective in mice still has a long way to go before it’s viable for use on humans, assuming it is ever viable to use on humans.
Mice and humans are quite different, and whilst it looks like this treatment actually reverses the effects of dementia in mice, it’s far from clear that it would have the same impact on humans. By the time people start exhibiting Alzheimer’s symptoms, the brain will already have sustained quite a lot of damage - by which I mean death of neurons - so it’s hard to see how this would actually reverse the disease, as opposed to simply slowing or halting its progression, without these neurons being replaced.
Most people start exhibiting Alzheimer's symptoms long before they develop full-blown Alzheimer's. Starting treatment when a person has only taken a small amount of damage, reversing what would go on to cause further damage, could be a really big deal.
Mice and humans are quite different, and whilst it looks like this treatment actually reverses the effects of dementia in mice, it’s far from clear that it would have the same impact on humans. By the time people start exhibiting Alzheimer’s symptoms, the brain will already have sustained quite a lot of damage - by which I mean death of neurons - so it’s hard to see how this would actually reverse the disease, as opposed to simply slowing or halting its progression, without these neurons being replaced.