It's more complex than just that. At CTAD just a couple of weeks ago there was a presentation on drugs that managed to reduce AB (biomarker was inferred by a PET scan) and it did not result in increased cognition.
A PET scan is not a biomarker. The Amyloid Beta (AB)* is the biomarker, the PET w/ tracer (such as the Pittsburg Compound Beta) are used to detected the biomarker.
It's also important to note that Amyloid Beta is only part of the problem. Neurofibrillary Tangles (NFT) are the primary biomarker of Alzheimer's Dementia, and happen inside the neurons. NFTs disable to ability for neurons to communicate with each other, and lead to the death of disabled neurons.
It is completely possible that we can't reverse AD, but can only slow it down / halt progression.
*Was it AB40 / AB42 / or a different Amyloid Beta?
A simple hypothesis which could explain this might be that the plaques cause effectivelt permanent brain damage. The question is whether degenerative patterns ceased or slowed after substantial clearing of plaques from the brain.
I would expect this test (and therefore the hypothesis) to fail if the plaques themselves are a byproduct rather than the cause of degradation in brain function. That said, I'm surprised I haven't read much in Gates' Notes or other funding sources on potential ties to HSV1 considering all the increasingly supportive research between the two.
They used several techniques that clear beta amyloid from the brain.(antibodies and ultrasound). And they've have little if any effect on cognition. I'm starting to think beta amyloid is a red herring, or maybe just important in the prodromal stages of the disease.
Another point is that a majority of Alzheimer's patients have other neurodegenerative conditions, with vascular dementia being one of the most common. So it is reasonable to expect that you can in fact meaningfully address Alzheimer's and see little to no improvement in a patient.
