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

Article type: Research Article

Authors: Lee, Yang Hyun^{a; 1} | Jeon, Seun^{b; 1} | Yoo, Han Soo^a | Chung, Seok Jong^a | Jung, Jin Ho^a | Baik, Kyoungwon^a | Sohn, Young H.^a | Lee, Phil Hyu^a | Yun, Mijin^c | Evans, Alan C.^b | Ye, Byoung Seok^{a; *}

Affiliations: [a] Department of Neurology, Yonsei University College of Medicine, Seoul, South Korea | [b] McGill Center for Integrative Neuroscience, Montreal Neurological Institute, McGill University, Montreal, Canada | [c] Department of Nuclear Medicine, Yonsei University College of Medicine, Seoul, South Korea

Correspondence: [*] Correspondence to: Byoung Seok Ye, MD, PhD, Department of Neurology, Yonsei University College of Medicine, 50-1 Yonsei-ro, Seodaemun-gu, Seoul, 03722, South Korea. Tel.: +82 2 2228 1609; Fax: +82 2 393 0705; E-mail: [email protected].

Note: [1] These authors contributed equally to this work.

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.

Keywords: Alzheimer’s disease, amyloid, glucose metabolism, lewy body disease

DOI: 10.3233/JAD-201094

Journal: Journal of Alzheimer's Disease, vol. 79, no. 4, pp. 1471-1487, 2021