There's a theory on beta amyloid that it's merely the by-product of other causative agents, and that as a surrogate end-point for Alzheimer's outcomes, it's not nearly as useful as symptom reduction, as you state. My professor who studied AD and dementia likened beta-amyloid to the garbage leftover in a stadium or outdoor concert: you know something went down, this leftover trash isn't great, but hard to determine what actually did occur just based on beta-amyloid.

Of course, the AD research field is still divided and there are many competing theories. Solving AD and dementia is one of the greatest challenges in modern science.

Plaque on your teeth is a symptom too:

Do what you can daily, but let a dentist break it up periodically.

It’s moving to a phase I trial, that means it’s just being tested for tolerability and adverse effects. A firm conclusion about outcome won’t be available until a phase III trial is completed, that’s years down the line. So we don’t know, but looks promising.

Assuming this gets "breakthrough therapy" designation how many years down the line will it be available ?

Well it's not a drug, and I assume that they're using previously approved medical devices to apply it. It seems to me to be more like a new surgical technique. In that case it may just be a matter of finding a physician willing to apply it, though without safety or efficacy data I would expect that number to be hovering around zero.

The information around Alzheimers seems to be heading the direction that the beta-amyloid plaques are an immune response to the HSV1 herpes virus that help prevent the spread of the virus.[1]

I suppose it can't be ruled out yet that this immune response could still cause damage, but it does make me wonder if the plaques are actually responsible at all for the symptoms seen, since like you said, other drugs reduce the plaques with no improvement in symptoms.

It's interesting that this treatment seems to work when others do not- when they seem to be accomplishing the same thing (reduction of beta-amyloid plaques)

[1] http://www.virology.ws/2018/11/08/herpes-simplex-virus-and-a...

Your claim is far too strong, that is merely one theory, evidenced by a posted link from/by/for virologists. There is not a field-wide consensus to support that by any stretch.

I don't think I made any strong claims myself? I guess "Seems to be heading the direction" implied too much of a consensus? The fact that antiviral drugs helped- does seem to lend a good amount of credence to the theory though?

I've just seen the theory come up a number of times, from a number of locations, in the past few months, so that gave me an impression that it was gaining ground.

It says more than that:

"the team has worked to further test and refine the technique, successfully proving the treatment both clears toxic proteins and restores memory function safely in several different rodent models, including an older mouse model designed to resemble human brains of 80 to 90 years old."