If you go digging around you'll find dozens of other similar results in the past five to ten years for dozens of various compounds, some of which produce larger effect sizes than this one. This is nothing to get excited over.
It is interesting the way in which various groups leap upon some research reports but not others. The challenge is always having the context for the broader state of research to understand whether it is meaningful or new or not.
The present mainstream view of Alzheimer's is that amyloid (and tau) clearance is the way to go. Immunotherapies are the most developed tool, but that is so far proving to be hard - it is too early to say whether failures in clinical trials are because it is hard or because amyloid clearance isn't as useful as thought in this condition. Which could be for any number of reasons including that amyloid-related biochemistry is the problem, but clearing a particular variant or stage of its aggregation doesn't touch that problem area.
Amyloid levels in the brain are in fact highly dynamic on a very short timescale. That Alzheimer's develops slowly supports the view that the condition is a slow degeneration of natural clearance mechanisms, such as the filtration performed by the choroid plexus, or the more recently investigated peristaltic passage of fluid out of the brain by other channels. E.g.:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4245362/
On that latter point, the Methuselah Foundation just a few days ago seed funded a startup company that will investigate whether reversing the degeneration of peristaltic fluid passage with aging will improve clearance and thus stop the progression of Alzheimer's. It's based on as yet unpublished work by Doug Ethell at GCBS Western who presented at Rejuvenation Biotechnology 2015 ( http://www.sens.org/files/conferences/rb2015/RB2015-Program.... ), and has the merit that it should be a fast failure if the theory is wrong, unlike many of the other efforts in Alzheimer's research.