Clinical and biomarker changes in sporadic Alzheimer's disease: Amyloid-β not useful marker for disease onset or progression

The failure of all anti-amyloid-β (Aβ) drugs has led to a debate about the central role of amyloid in sporadic Alzheimer9s disease (SAD). In order to resolve this issue, it is necessary to evaluate the impact of Aβ biomarkers on SAD by measuring the dynamic changes in biomarkers and clinical profiles in the progression of SAD. We identified a clearer picture of the clinical and biomarker changes in the progression of SAD by aligning the clinical diagnosis of mild cognitive impairment (MCI) or AD onset. We found that changes in hippocampal volume and FDG, rather than Aβ biomarkers, were associated with the changes in clinical measures in the progression of SAD. In addition, cognitively normal people with elevated and with normal amyloid showed no significant differences in clinical measures, hippocampal volume, or FDG. This study reveals that Aβ is not a useful biomarker for predicting the clinical progression of patients who develop SAD.