Clinical and biomarker changes in sporadic Alzheimer’s disease

Abstract

32The failure of all anti-amyloid-β (Aβ) drugs has led to a debate about the central role of amyloid 33 in sporadic Alzheimer's disease (SAD). In order to resolve this issue, it is necessary to evaluate 34 the impact of Aβ biomarkers on SAD by measuring the dynamic changes in biomarkers and 35 clinical profiles in the progression of SAD. We identified a clearer picture of the clinical and 36 biomarker changes in the progression of SAD by aligning the clinical diagnosis of mild cognitive 37 impairment (MCI) or AD onset. We found that changes in hippocampal volume and FDG, rather 38 than Aβ biomarkers, were associated with the changes in clinical measures in the progression of 39 SAD. In addition, cognitively normal people with elevated and with normal amyloid showed no 40 significant differences in clinical measures, hippocampal volume, or FDG. This study reveals 41 that Aβ is not a useful biomarker for predicting the clinical progression of patients who develop 42 SAD. 43 44