The mainstream theory is that Alzheimer’s is caused by the buildup of beta amyloid proteins in the brain into large deposits.
These deposits, also called plaques, have been a physiological hallmark ever since Alois Alzheimer autopsied brains of people who died with this form of dementia.
Crenezumab was supposed to work in accordance with the mainstream theory.
Clear out the plaques and you stop the progression of Alzheimer’s.
But crenezumab’s failure indicates there’s more to curing Alzheimer’s than just clearing out these plaque deposits.
Profiting off Failure
There’s one company using what was learned from crenezumab’s failure.
This company’s scientists have identified that garden-variety amyloid proteins aren’t the problem.
Specifically, it’s mutated, twisted, misfolded toxic variants. According to this idea, misfolded proteins act like prions, meaning they essentially “infect” normal forms of beta amyloid, turning them into toxic versions as well.
To that end, this company is developing highly specific, targeted therapies based on monoclonal antibodies engineered in a lab.
They are working on engineered antibodies that target these misfolded variants specifically, tagging them for immune system clearance.
This specificity should allow for higher dosing and greater clearance of toxic species of this protein.
If it works, it will be a historic victory.
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