The issue is that that Amyloid has been seen as causative, when in reality the beta-amyloid deposits appear to be a pathological and possible an immune response in many, but not all, patients that are diagnosed with AD.
The plaque removal drug attempts fail because they do not address the issue or issues upstream of the beta-amyloid deposits. Despite the recently aborted BP attempts at amyloid removal some, possibly in error, cling on to the idea that treating early with plaque preventing drugs may delay or avoid the onset of a clinical AD diagnosis.
So beta-amyloid may be a biomarker of AD at some point in disease progression, but not necessarily a good early signal.
As a biomarker Amyloid might be useful e.g. for Anavex A2-73 or A3-71 to be taken early or perhaps still as a prophylactic. This because it would appear that a growing number of researchers, independent of Anavex, conclude that the Sigma-1 receptor is a potent drug target upstream of neurodevelopmental and neurodegenerative disease.
Check out my recent two posts with YouTube presentations.