RichardS wrote:I, too, was baffled when I thought I heard Holtzman say we are unsure whether increasing or decreasing apoe would be therapeutic. I may have to chalk that one up to misunderstanding him. As Stavia said, a lot of it was above my pay grade and many of the speakers talked at a pace that left me behind. Still, I think it was encouraging that apoe levels were mentioned in the context of possible therapies.
Holtzman very much believes that decreasing apoE levels is the way to go for treating Alzheimer's, but there are others who believe just as strongly that increasing apoE levels is the way to go. Many pharma companies pursed LXR agonists, which increase apoE levels, but they never got past Phase I due to toxicity. If he was being even handed, it's quite possible that Holtzman could have said he was unsure about increasing or decreasing levels.
I'm surprised Jeff Cummings didn't say anything about his bexorotene trial when you asked him about apoE related therapies. Of course that trial looks like it didn't really work, but it was not very well powered to begin with.