Plaques, however, do lead to an aggravated response by the immune-equivalent cells in the brain (microglia). There has been a lot of interest in how much this microglia response to plaques triggers some of the symptoms of AD, and this what the research summarised in TFA is interested in also. Despite what TFA implies (it's an overcooked Uni press release) there's been heaps of interest in microglia over the last few years in the AD space.
Ultimately, we still don't know what causes the majority of AD symptoms, and this is a very controversial space. Historically, a number of AD researchers (including one very prominent researcher) staked their reputation on plaques being fully or mostly causative, and refuse to let go of this idea despite the growing body of contrary evidence -- which has created a bit of cognitive hysteresis in the field (and led to vast amounts of arguably wasted pharma R&D). It was a good idea at the time as it was the obvious, most parsimonious explanation; but biological reality has a habit of not conforming with Occam's razor, sadly.
(As for terminal lucidity -- this is not my field; IIUC it's also debated, but your idea is not entirely at odds with one theory. There are many theories, and it's not entirely accepted that this even reliably occurs at all.)
So this study ties in neatly with that.
Is this actually the case or are you conjecturing?
My guess is that there are a large set of genetic, environmental, and idiopathic contributors that converge to a loosely similar phenotype, but couldn't be treated effectively in the same way because they have different sets of causes.
I think we'll eventually get to a point where we can treat many kinds of dementia in the same way we treat infections/etc... But it'll take a while.