Prediction of amyloid‐beta accumulating normal cognitive elderly

Abstract

Background: Amyloid-β (Aβ) accumulation, a major biomarker in Alzheimer's disease (AD), induces tau accumulation, eventually resulting in cognitive decline. However, Aβ trajectory in cognitively normal participants has not been extensively investigated, yet.Modeling of Aβ trajectory remains an important goal, as future treatments targeting Aβ are expected to be developed. In the present study, we therefore investigated whether they might be divided into the normal aging group and the pathological group with increased amyloid. We also compared the differences between the non-accumulating group and accumulating group. Method: We included 297 subjects from the Alzheimer's Disease Neuroimaging Initiative database, who showed normal cognition at baseline. All subjects underwent neuropsychological test, apolipoprotein E (APOE) genotype test, brain MRI, and an average of 3.03 follow-up 18 F-florbetapir (AV45) PET scans. The original dataset was divided by 6:4 to create a training set and a validation set. Latent Class Growth Analysis was used for statistical analysis.Result: Based on the information criterion, the model consisting of three classes was found to be the best with a high entropy of 0.979: class 1 (non-accumulating group; n = 117, 65.7%), class 2 (accumulating group; n = 46, 25.8%), and class 3 (high accumulation group; n = 15, 8.4%) (Figure). The accumulating group had more APOE ε4 carriers and a higher tau burden than the non-accumulating group (Table ). Conclusion:Our study showed that there is the heterogeneity of Aβ trajectories according to aging in the normal cognitive elderly. Heterogeneity of Aβ accumulation and early detection of accumulating group may be helpful in early diagnosis and treatment of AD.