After the disaster known as bapineuzumab Phase III, I think it’s time to seriously question whether clearing amyloid beta deposits from the brain has any therapeutic benefit to Alzheimer’s patients. The bapi Phase III results speak with a resounding “No”. We are still awaiting Phase III results from Eli Lilly’s solanezumab, but the current prognosis for solanezumab results are about the same as with bapineuzumab.
Looking at the larger picture, I think that the communities of neuroscience research and pharmaceutical companies might need to do some serious soul searching on whether they have been racing down an amyloid blind alley.
Respected scientists, and drug company executives, are just as susceptible to cognitive dissonance as the rest of us. It’s much easier to choose one belief and stick with it (even when it might be wrong), rather than actively consider and pursue alternate ideas.
The real tragedy here is the wasted time not pursuing alternate hypotheses (such as hyperphosphorylated tau), with the same resources and vigor that have been afforded to the amyloid hypothesis over the past decade.
I believe we’ll eventually find a solution to the Alzheimer’s Dementia problem (a drug that can delay symptom onset for 10 years would be hailed as a huge success), but I think that the Alzheimer’s research community might need to issue a tacit mea culpa, and begin shifting major resources away from amyloid towards other research avenues.