I am forever fascinated by how often -- in human biology -- it seems that any given cognitive function disease/impairment is driven not by one or two clear defining change(s), in brain chemistry, or its DNA replication process -- but by perhaps thousands (or tens of thousands?) tiny, almost imperceptible ones. . . occuring seemingly almost at random. That, my friends, will likely make Alzheimer’s one very tough problem to solve.
Do go read all of Matt's take -- but I'd be a little concerned, if I were looking at Merck's current very high-spend R&D program, almost exclusively aimed at a pill for the Alzheimer’s Beta Amyloid pathway. Here's a bit from Matt:
. . . .Here’s what may make scientists working on Alzheimer’s disease nervous, though. Eli Lilly had noted a reason for hope when its Alzheimer’s antibody failed: it seemed to work in patients with mild Alzheimer’s disease, and not in those who had the more severe moderate form of the disease. Lilly is continuing to develop its drug.I do not mean to sound overly-alarmist -- and it is not (yet) time to drop any of the other programs -- but it is very clear that we know less about Alzheimer’s than we thought, before this morning.
It would be comforting if the Baxter trial had found the same thing. That would mean that this approach was consistently working in the same group of patients Instead, Baxter says it is seeing efficacy in the moderate form of the disease. This is more in line with what you’d expect if targeting beta amyloid resulted in only slight benefits or none at all. There will probably be more information as Baxter scientists continue to look at the results. . . .
2 comments:
While there are approved drug treatments available for AD, such as the cholinesterase inhibitors, these unfortunately aren’t disease-modifying; they treat the symptoms rather than the cause of the disease. At best, an AD patient might expect a 6-12 month delay in the worsening of symptoms. There are a number of ongoing drug trials that are aiming to target what many see as central to Alzheimer’s disease, namely the toxic β-amyloid peptide that accumulates in the brains of patient’s with AD. Unfortunately, the results from these aren’t too promising. Some of the trials have shown a reduction in β-amyloid but unfortunately without any corresponding improvement in symptoms.
Toronto memory clinic
Thanks Toronto! --
And, obviously the immediately above views are those of the author of the comment -- not necessarily mine.
I do appreciate the insights -- do stop back!
Namaste
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