Granted, I have heard a scientist (in an unrelated field, I think it was some astronomical NPR interview) describe science as a bit like a supertanker...there usually is some prevailing thing that everyone believes in, but as contrary evidence piles up, the direction slowly turns.
I guess my own question is whether Alzheimer's/amyloid thinking was atypically stuck on one hypothesis, vs. is this just the slow pace of progress as usual for a given field? I mean...it's not like the amyloid deposition isn't there...
I only play a AD expert on TV (haha I jest...I like to say this because I had no intention of specializing in this when I was training but, hey, in the real world, you have to treat the "market" that rolls in the door....). I work more in the Parkinson's world, and while I would say there are cliques, which do affect who gets NIH (or used to get...I have no idea what's going on there now...), I can't say there's one prevailing "cabal" that's obsessed with any one direction. the bigger issue is that current Parkinson's research is a bit scattershot in too many directions.
My other pet peeve is somewhat unrelated, where the article mentions other directions like neuroinflammation and oxidative stress; the problem is these are also vague/broad topics, that have been thrown around like panaceas for every disease from head to toe; my own superstition is that when a new drug candidate comes out for "neuroinflammation" or "oxidative stress", I'd bet a healthy bunch of nickels it won't amount to much.
in short, and off the top of my head, not in a few years.
GLP-1 (exenatide trial) failed to show benefit Phase 3
prasinezumab (synuclein targeted monoclonal ab) also have not been impressive although I think Novartis is chasing after some statistical signals that popped up in secondary endpoints
there is some academic chatter I heard about elucidating more the process of how normal synuclein turns into the abnormal insoluble form, so that might be the most promising direction.
A couple new stem cell implant trials but not sure if they solved the big problems w/ the last trials - the stem cells eventually develop parkinsonian features, and also it doesn't replace the connectivity/networks that is lost.
Other big question is really what starts the process in the first place since symptomatic patients at initial diagnosis now thought to have been "preclinical" w/ prodromal form for several years...we still don't know.
I guess my own question is whether Alzheimer's/amyloid thinking was atypically stuck on one hypothesis, vs. is this just the slow pace of progress as usual for a given field? I mean...it's not like the amyloid deposition isn't there...
I only play a AD expert on TV (haha I jest...I like to say this because I had no intention of specializing in this when I was training but, hey, in the real world, you have to treat the "market" that rolls in the door....). I work more in the Parkinson's world, and while I would say there are cliques, which do affect who gets NIH (or used to get...I have no idea what's going on there now...), I can't say there's one prevailing "cabal" that's obsessed with any one direction. the bigger issue is that current Parkinson's research is a bit scattershot in too many directions.
My other pet peeve is somewhat unrelated, where the article mentions other directions like neuroinflammation and oxidative stress; the problem is these are also vague/broad topics, that have been thrown around like panaceas for every disease from head to toe; my own superstition is that when a new drug candidate comes out for "neuroinflammation" or "oxidative stress", I'd bet a healthy bunch of nickels it won't amount to much.