This is a crucial question.
After debilitating accumulations of waste proteins (amyloids and tau tangles) have disabled neurons for lengthy periods, when Alzheimer's pathologies are fully present (dementia, etc.), could blarcamesine facilitate or cause the clearance of these proteins, and thereby restore normalized neuron functions?
Perhaps. But probably not, inasmuch as blarcamesine does not directly react with or connect or clear waste proteins.
The key test would be this. Provide two critical measures in blarcamesine therapy for Alzheimer's.
First, yet to be precisely determined, administer an adequate dose of the drug. Without enough of it (inside neurons), there is no way it could work.
But equally important would be the early administration of the drug; BEFORE the waste proteins that cause Alzheimer's symptoms have begun to profusely accumulate; before they essentially crystalize or otherwise agglutinate in neurons and nerves. With early, first-indication dosing, the drug's ability to restore normalized waste-clearing neuron chemistries can be effective. The amyloid and tau wastes are cleared before they further accumulate --- exactly as in the case of people who don't yet have any Alzheimer's symptoms. Protein wastes are generated in all neurons, at all ages. Properly functioning neurons have chemical mechanisms to clear those wastes before they accumulate. By its activation of the sigma-1 receptor, blarcamesine can facilitate all of the normal, downstream chemical pathways that normally clear protein wastes.
This slides blarcamesine into the category of an Alzheimer's prophylactic; a drug that prevents the untoward development or progression of the disease.
The applicable phrase? Enough, early on!
Are these two factors being effectively implemented in any Alzheimer's/blarcamesine trial? Until they are, the determinative answers to blarcamesine efficacies against Alzheimer's will not be known.
