Here’s an interesting look at the current state of the Alzheimer’s field from Bloomberg. The current big hope is Wyeth (and Elan)’s bapineuzumab, which I last wrote about here. That was after the companies reported what had to be considered less-than-hoped-for efficacy in the clinic. The current trial is the one sorted out by APOE4 status of the patients. After the earlier trial data, it seems unlikely that there’s going to be a robust effect across the board – the people with the APOE4 mutation are probably the best hope for seeing real efficacy.
And if bapineuzumab doesn’t turn out to work even for them? Well:
“Everyone is waiting with bated breath on bapineuzumab,” said Michael Gold, London-based Glaxo’s vice president of neurosciences, in an interview. “If that one fails, then everyone will say we have to rethink the amyloid hypothesis.”
Now that will be a painful process, but it’s one that may well already have begun. beta-Amyloid has been the front-runner for. . .well, for decades now, to be honest. And it’s been a target for drug companies since around the late 1980s/early 1990s, as it became clear that it was produced by proteolytic cleavage from a larger precursor protein. A vast amount of time, effort, and money have gone into trying to find something that will interrupt that process, and it’s going to be rather hard to take if we find out that we’ve been chasing a symptom of Alzheimer’s rather than a cause.
But there’s really no other way to find such things out. Human beings are the only animals that really seem to get Alzheimer’s, and that’s made it a ferocious therapeutic area to work in. The amyloid hypothesis will die hard if die it does.