The prevalence and biomarkers’ characteristic of rapidly progressive Alzheimer's disease from the Alzheimer's Disease Neuroimaging Initiative database

Alzheimer's and Dementia: Translational Research and Clinical Interventions - Tập 3 - Trang 107-113 - 2017
Maowen Ba1,2, Xiaofeng Li2,3, Kok Pin Ng2,4, Tharick A. Pascoal2, Sulantha Mathotaarachchi2, Pedro Rosa-Neto2, Serge Gauthier2
1Department of Neurology, Yantai Yuhuangding Hospital Affiliated to Qingdao Medical University, Shandong, People’s Republic of China
2Alzheimer's Disease Research Unit, McGill Centre for Studies in Aging, McGill University, Douglas Institute, Montreal, Quebec, Canada
3Department of Neurology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, People’s Republic of China
4Department of Neurology, National Neuroscience Institute, Singapore

Tóm tắt

AbstractIntroductionThe prevalence and detailed biomarkers’ characteristic of rapidly progressive Alzheimer's disease (rpAD) remain incompletely understood.MethodsA total of 312 mild AD patients from the Alzheimer's Disease Neuroimaging Initiative database were chosen and dichotomized into rpAD and non‐rpAD groups. We performed the prevalence and comprehensive biomarker evaluation.ResultsThe prevalence of rpAD was 17.6% in mild AD. Compared with non‐rpAD, there were no differences in APOE ε4/ε4, APOE ε3/ε4, and APOE ε2/ε4 genotype distribution, cerebrospinal fluid tau, phosphorylated tau (p‐tau), amyloid‐β, hippocampus volume, and amyloid deposition in rpAD. Yet, a lower p‐tau/tau ratio was observed in rpAD (P = .04). rpAD showed region‐specific hypometabolism ([18F]fluorodeoxyglucose‐positron emission tomography [FDG‐PET]) (P = .001). Receiver‐operating characteristic analysis of FDG‐PET demonstrated that left angular and left temporal cortices were the regions with higher area under the curve and predictive value for identifying clinical at‐risk rpAD.DiscussionWe identified that rpAD commonly existed in mild AD. Cerebral hypometabolism could provide potential clinical differential value for rpAD in the short‐term follow‐up period.

Tài liệu tham khảo

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Alzheimer's and Dementia: Translational Research and Clinical Interventions

Tập 3

107-113

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