Effect of Alzheimer's Disease and Lewy Body Disease on Metabolic Changes

Yang Hyun Lee, Seun Jeon, Han Soo Yoo, Seok Jong Chung, Jin Ho Jung, Kyoungwon Baik, Young H. Sohn, Phil Hyu Lee, Mijin Yun, Alan C. Evans, Byoung Seok Ye

Research output: Contribution to journalArticlepeer-review

Abstract

Background: The relationship among amyloid-β (Aβ) deposition on amyloid positron emission tomography (PET), cortical metabolism on 18F-fluoro-2-deoxy-D-glucose (FDG)-PET, and clinical diagnosis has not been elucidated for both Alzheimer's disease (AD) and Lewy body disease (LBD). Objective: We investigated the patterns of cerebral metabolism according to the presence of AD and LBD. Methods: A total of 178 subjects were enrolled including 42 pure AD, 32 pure LBD, 34 Lewy body variant AD (LBVAD), 15 LBD with amyloid, 26 AD with dementia with Lewy bodies (DLB), and 29 control subjects. Pure AD, LBVAD, and AD with DLB groups had biomarker-supported diagnoses of typical AD, while pure LBD, LBD with amyloid, and AD with DLB groups had biomarker-supported diagnoses of typical LBD. Typical AD and LBD with amyloid showed amyloid-positivity on 18F-florbetaben (FBB) PET, while typical LBD and LBVAD had abnormalities on dopamine transporter PET. We measured regional patterns of glucose metabolism using FDG-PET and evaluated their relationship with AD and LBD. Results: Compared with control group, typical AD and typical LBD commonly exhibited hypometabolism in the bilateral temporo-parietal junction, precuneus, and posterior cingulate cortex. Typical AD showed an additional hypometabolism in the entorhinal cortex, while patients with dopamine transporter abnormality-supported diagnosis of LBD showed diffuse hypometabolism that spared the sensory-motor cortex. Although the diffuse hypometabolism in LBD also involved the occipital cortex, prominent occipital hypometabolism was only seen in LBD with amyloid group. Conclusion: Combining clinical and metabolic evaluations may enhance the diagnostic accuracy of AD, LBD, and mixed disease cases.

Original languageEnglish
Pages (from-to)1471-1487
Number of pages17
JournalJournal of Alzheimer's Disease
Volume79
Issue number4
DOIs
Publication statusPublished - 2021

Bibliographical note

Funding Information:
This research was supported by a faculty research grant from Yonsei University College of Medicine (6-2018-0052) and the National Research Foundation of Korea Grant funded by the Korean government (NRF-2019R1I1A1A01059454), and grants from the Canadian Institute of Health Research (CIHR; 201085 and 247003) and Brain Canada/FNC (238990) awarded to Alan C. Evans. Seun Jeon is the recipient of the following fellowships that contributed to his support: Bourse Fonds de Recherche Sant? Qu?bec (FRQS, dossier 34240 and 259605) and by Jeanne Timmins Costello Fellowship of the Montreal Neurological Institute (240522).

Publisher Copyright:
© 2021 - IOS Press. All rights reserved.

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)
  • Clinical Psychology
  • Geriatrics and Gerontology
  • Psychiatry and Mental health

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