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Zhuo J, Zhang Y, Liu Y, et al. New Trajectory of Clinical and Biomarker Changes in Sporadic Alzheimer's Disease. Cereb Cortex. 2021;31(7):3363-3373doi: 10.1093/cercor/bhab017.
Zhuo, J., Zhang, Y., Liu, Y., Liu, B., Zhou, X., Bartlett, P. F., Jiang, T. (2021). New Trajectory of Clinical and Biomarker Changes in Sporadic Alzheimer's Disease. Cerebral cortex (New York, N.Y. : 1991), 31(7), 3363-3373. https://doi.org/10.1093/cercor/bhab017
Zhuo, Junjie, et al. "New Trajectory of Clinical and Biomarker Changes in Sporadic Alzheimer's Disease." Cerebral cortex (New York, N.Y. : 1991) vol. 31,7 (2021): 3363-3373. doi: https://doi.org/10.1093/cercor/bhab017
Zhuo J, Zhang Y, Liu Y, Liu B, Zhou X, Bartlett PF, Jiang T. New Trajectory of Clinical and Biomarker Changes in Sporadic Alzheimer's Disease. Cereb Cortex. 2021 Jun 10;31(7):3363-3373. doi: 10.1093/cercor/bhab017. PMID: 33690839.
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Cereb Cortex. 2021 Jun 10;31(7):3363-3373. doi: 10.1093/cercor/bhab017.

New Trajectory of Clinical and Biomarker Changes in Sporadic Alzheimer's Disease.

Cerebral cortex (New York, N.Y. : 1991)

Junjie Zhuo, Yuanchao Zhang, Yong Liu, Bing Liu, Xiaoqing Zhou, Perry F Bartlett, Tianzi Jiang,

Affiliations

  1. Brainnetome Center, Institute of Automation, Chinese Academy of Sciences, Beijing 100190, China.
  2. The Queensland Brain Institute, University of Queensland, Brisbane, QLD 4072, Australia.
  3. School of Biomedical Engineering, Hainan University, Haikou 570228, China.
  4. The Clinical Hospital of Chengdu Brain Science Institute, MOE Key Lab for Neuroinformation, University of Electronic Science and Technology of China, Chengdu 625014, China.
  5. University of Chinese Academy of Sciences, Beijing 100049, China.
  6. CAS Center for Excellence in Brain Science, Institute of Automation, Chinese Academy of Sciences, Beijing 100190, China.

PMID: 33690839 DOI: 10.1093/cercor/bhab017

Abstract

Identifying dynamic changes in biomarkers and clinical profiles is essential for understanding the progression of Alzheimer's disease (AD). The relevant studies have primarily relied on patients with autosomal dominant AD; however, relevant studies in sporadic AD are poorly understood. Here, we analyzed longitudinal data from 665 participants (mean follow-up 4.90 ± 2.83 years). By aligning normal cognition (CN) baseline with a clinical diagnosis of mild cognitive impairment (MCI) or AD, we studied the progression of AD using a linear mixed model to estimate the clinical and biomarker changes from stable CN to MCI to AD. The results showed that the trajectory of hippocampal volume and fluorodeoxyglucose (FDG) was consistent with the clinical measures in that they did not follow a hypothetical sigmoid curve but rather showed a slow change in the initial stage and accelerated changes in the later stage from MCI conversion to AD. Dramatic hippocampal atrophy and the ADAS13 increase were, respectively, 2.5 and 1 years earlier than the MCI onset. Besides, cognitively normal people with elevated and normal amyloid showed no significant differences in clinical measures, hippocampal volume, or FDG. These results reveal that pre-MCI to pre-AD may be a better time window for future clinical trial design.

© The Author(s) 2021. Published by Oxford University Press. All rights reserved. For permissions, please e-mail: [email protected].

Keywords: biomarker trajectories; hippocampal volume; mild cognitive impairment; sporadic Alzheimer’s disease; β-amyloid

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