There is a myriad of Alzheimer’s drugs. Each of them has a therapeutic target. Just a molecule or a receptor. The question is how far-reaching waves the drug makes in the patient’s physiology? Are they localized like as in the case of Donezepil; just availability of a neurotransmitter at synapses or system-wide?
CATD 2019 for $AVXL is the moment when the company might prove that beyond the data from the trials there is a cascade of changes from cognition to plaque in brain and gut biome together altering the etiology of Alzheimer’s.
I get on a limb when I suppose that the imaging which, one of the presentations lists, is aimed at measuring the disappearance of plaque after 104 weeks of dosing, and not the thickness of the cortex. If this would be true because the plaque is the only biomarker of the disease detectable and approved by FDA then it could be beginning of acceptance by the medical establishment that Blarcamesine is the drug that has been eluding the industry for years.
If indeed this is the case then this is Ignaz Semmelweise moment! I hope $AVXL is not going to end up like him, but the powers that be…
This would be seminal.
The gut biome is interesting but not that seminal from the point of view of the resistance by the medical establishment as right now it is relegated to be a side story. It is now obvious that it is the inflammation that does the most irreparable damage to brains of the patients. The question now is: Does Blarcamesine control inflammation by lowering plaque deposits or lowering system-wide inflammation? Another would be: Is the brain condition affecting biome or lowering inflammation in the gut alters biome? Is the biome directly affected by Blarcamesine?
Read the story of Ignaz Semmelweis, since history rhymes.
$1.00 is about one bottle so .....please contribute..