Eli Lilly Pharmaceuticals has stopped trials of a new drug, semagacestat, which was developed to reduce beta amyloid plaques in the brain, because subjects who took the drug showed a worsening cognitive decline. (http://www.nytimes.com/2010/08/18/business/18lilly.html?_r=1&th&emc=th)
This was an unexpected result, and follows the recent failures of Alzheimer drug trials by a Pfizer/Medivation team, and by Myriad Genetics.
One of the lead researchers speculated that “too much reduction in amyloid beta” might be unexpectedly harmful.
Which leads me to wonder: Could there be something about amyloid beta that enhances cognition in lesser quantities (i.e., a little bit is good, a lot is bad)? Another question comes to mind: Is amyloid beta really the culprit or is it a “waste product” of the degenerative process?
The researchers understand these concepts better than I, but nevertheless it is clear that this is a trickier problem to “untangle” than people had hoped. This is also why my frequent “pessimistic” comments about curing Alzheimer’s are more pragmatic than pessimistic.
One more question: What’s with the increasingly bizarre taxonomy of generic drug names that are impossible to pronounce, let alone remember? Have we really run out of simpler names, or is this a ploy by Big Pharma to make low-cost generics harder to market down the road?