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.