Okay, I admit it--even an optimist like me, who subtitles her book, "the good news from the front lines of memory research," was distressed when Myriad Pharmaceuticals announced the other day that its promising drug, Flurizan, had failed its Phase 3 clinical trial, and that the company, which had invested millions in it, was closing the door and walking away. Meanwhile, the Danish drug company that, the week before, had inked a deal distribute Flurizan in Europe, a move that, at the time, raised hopes that the Phase 3 trial results looked good, was out millions of dollars. It was lose, lose, lose, all around, expecially for the patients and their families.

As soon as the Flurizan news broke, there was an almost immediate backlash against the theory that had prompted the development of the drug in the first place, what is known in the field as the amyloid hypothesis. Among other things, the amyloid hypothesis suggests that AD is caused by too much of a toxic peptide in the brain called beta amyloid 42 (abeta 42), and that if a drug could either clear it or prevent its production, AD would be arrested. There are many reasons why the amyloid hypothesis is compelling, so when Flurizan failed, it seemed like a much bigger failure, one not only of a single drug, but of an entire approach. If the approach was wrong, then much of the field was wrong, and all the progress of the last five years was illusory.