Not an expert, but I read Derek Lowe's blog[1] and he tends to report on pretty much all the drug trials in the Alzheimer's space.
The amyloid hypothesis (that the cause of Alzheimers is the buildup of beta amyloid plaques) seems pretty weak at this point. The drugs that remove or reduce amyloid buildup don't seem to stop the progression of the disease. The current best guess seems to be that the amyloid plaques are a symptom of whatever the underlying cause is. And the key takeaway is that we have NO IDEA what the actual cause is. We've got a bunch of guesses. One of them might even be right. Or possibly multiple, there are probably several diseases that cause the same symptoms.
So if we can detect the non-presence of amyloid plaques but detect symptoms that would be good as a way to distinguish between the different diseases. Of course there might be more than two variants...
I'll admit I wasn't aware in the 1980s when the hypothesis took hold, but it never seemed like a good one to me just because amyloids are so thermodynamically favored. There must be constant and diverse measures functioning correctly to avoid their formation.
>"Of all the myriad way a protien can fold, it happens to find one that induces the same malformation when it interacts with another protein."
It doesn't really "just happen", amyloids consist of peptides folded into beta-sheets and aggregates of these seem to be the most thermodynamically stable structures it is possible for polypeptide chains (regardless of sequence) to form:
"From a wide range of in vitro experiments on peptides and proteins we now know that the formation of amyloid structures is not a rare phenomenon associated with a small number of diseases but rather that it reflects a well-defined structural form of the protein that is an alternative to the native state — a form that may in principle be adopted by many, if not all, polypeptide sequences
[...]
These observations, therefore, have led to the remarkable conclusion that, at the concentrations present in living systems, the native states may not always represent the absolute free energy minima of the corresponding polypeptide chains — the native form of a protein could in some cases simply be a metastable monomeric (or functionally oligomeric) state that is separated from its polymeric amyloid form by high kinetic barriers" http://www.ncbi.nlm.nih.gov/pubmed/24854788
The amyloid hypothesis (that the cause of Alzheimers is the buildup of beta amyloid plaques) seems pretty weak at this point. The drugs that remove or reduce amyloid buildup don't seem to stop the progression of the disease. The current best guess seems to be that the amyloid plaques are a symptom of whatever the underlying cause is. And the key takeaway is that we have NO IDEA what the actual cause is. We've got a bunch of guesses. One of them might even be right. Or possibly multiple, there are probably several diseases that cause the same symptoms.
So if we can detect the non-presence of amyloid plaques but detect symptoms that would be good as a way to distinguish between the different diseases. Of course there might be more than two variants...
[1] http://blogs.sciencemag.org/pipeline/archives/category/alzhe...