I do sincerely hope that we find something for Azheimer's, but there's just a mountain of data suggesting that mouse models of Alzheimer's and/or ABeta simply not that useful.
But treating symptoms, esp restoring cognitive function, is a good thing.
The problem with the amyloid-beta hypothesis was the assumption that these plaques were causing the Alzheimers and that removing them by itself could lead to a cure.
This has been demonstrated for many years. And yet we waste literally billions per year researching treatments that will only work in mice. And yet we regularly publish articles proclaiming that we can cure mice, humans are next!
This research is BS and a waste of taxpayer money.
Alzheimer's patients often respond positively to exogenous ketone esthers, and a ketogenic diet. The proposed mechanism for this is that ketones are transported across the BBB differently than glucose. Even if glucose is unable to be transported into the brain, ketones often still are. Now that there is a drug to repair the BBB (and likely glucose transport as well), I expect the funding will mysteriously show up to properly investigate the "brain diabetes" theory of Alzheimers.
There is also increasing evidence that a healthy gut microbiome is necessary to maintain BBB integrity, both in development and aging.[38][39][40][41]
I'll drink to that (kefir)!
317070•36m ago
"Cognitive assessments revealed that treated AD mice exhibited significant improvements in spatial learning and memory, with performance levels comparable to those of wild-type mice. These cognitive benefits persisted for up to 6 months post-treatment."
I'm curious if Derek Lowe will comment on this on his blog. I'll await his opinion on how much we ought to celebrate here. He's not a big fan of the amyloid hypothesis and has worked many years in this exact field, so I reckon he will point out why skepsis is warranted.
underdeserver•26m ago