But it seems to come down to two simple concepts, which I call the tau of plaques. (My grandfather died of this disease, and given reader reaction last time I used this picture I figured it was worth using again.)
For clinicians it's actually an either-or, tau or plaques? Should drugs aim at the beta amyloid plaques we know are the cause of the disease, or the tau tangles which are its direct manifestation?
The big news of the last year is studies showing that perhaps focus should shift, away from the plaques and toward the tau. Unfortunately these are "mid-stage" studies, with a small number of patients, so no conclusion can yet be drawn.
Wall Street has bet heavily on the plaques, specifically a drug called Bapineuzumab which reduces them. But early results here are not promising, and despite the attempts by Wyeth and Elan to spin them, Wall Street is no longer so impressed.
A BBC story which came out this week showed that attacking the tau tangles may have more promise. More important, perhaps, is that the drug being tested, methylthioninium chloride, is based on methylene blue, a chemical dye with many other uses.
But there were only 321 people in the Rember study, 80 at each of three doses of Rember and a placebo group.
So that's where we are. We can fight the plaques. We can fight the tau. But can we really cure the disease? Maybe. And considering how fast the disease is catching on, we need to turn a maybe into a yes fast.