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Neurology, First published December 30, 2021 | DOI: https://doi.org/10.1212/WNL.0000000000013277 Association of β-Amyloid and Basal Forebrain With Cortical Thickness and Cognition in Alzheimer and Lewy Body Disease Spectra

Han Soo Yoo, MD¹, Seun Jeon, PhD^1,2, Enrica Cavedo, PhD^3,4, MinJin Ko, BS⁵, Mijin Yun, MD, PhD⁶, Phil Hyu Lee, MD, PhD¹, Young H. Sohn, MD, PhD¹, Michel J. Grothe, PhD^7,8, Stefan Teipel, MD^7,9, Harald Hampel, MD, PhD³, Alan C. Evans, PhD¹⁰ and Byoung Seok Ye, MD, PhD^1,*

¹Department of Neurology, Yonsei University College of Medicine, Seoul, South Korea
²Brain Research Institute, Yonsei University College of Medicine, Seoul, South Korea
³Sorbonne University, GRC n° 21, Alzheimer Precision Medicine (APM), AP-HP, Pitié-Salpêtrière Hospital, Boulevard de l'hôpital, F-75013, Paris, France
⁴Qynapse, Paris France
⁵Severance Biomedical Science Institute, Yonsei University College of Medicine, Seoul, South Korea
⁶Department of Nuclear Medicine, Yonsei University College of Medicine, Seoul, South Korea
⁷German Center for Neurodegenerative Diseases (DZNE) - Rostock/Greifswald, Rostock, Germany
⁸Unidad de Trastornos del Movimiento, Servicio de Neurología y Neurofisiología Clínica, Instituto de Biomedicina de Sevilla, Hospital Universitario Virgen del Rocío/CSIC/Universidad de Sevilla, Seville, Spain
⁹Department of Psychosomatic Medicine, University Medicine Rostock, Germany
¹⁰McGill Center for Integrative Neuroscience, Montreal Neurological Institute, McGill University, Montreal, Canada

Equal Author Contributions: Han Soo Yoo and Seun Jeon contributed equally to this work.

^*Corresponding Author: Byoung Seok Ye

Abstract

Objective: Cholinergic degeneration and β-amyloid contribute to brain atrophy and cognitive dysfunction in Alzheimer’s disease (AD) and Lewy body disease (LBD), but their relationship has not been comparatively evaluated.

Methods: In this cross-sectional study, we recruited 28 normal controls (NC), 55 patients with AD mild cognitive impairment (MCI), 34 patients with AD dementia, 28 patients with LBD MCI, and 51 patients with LBD dementia. The subjects underwent cognitive evaluation, brain magnetic resonance imaging to measure the basal forebrain (BF) volume and global cortical thickness (CTh), and 18F-Florbetaben (FBB) positron emission tomography to measure the standardized uptake value ratio (SUVR). Using general linear models and path analyses, the association of FBB-SUVR and BF volume with the CTh and/or cognitive dysfunction were evaluated in AD spectrum (AD and NC) and LBD spectrum (LBD and NC), respectively. Covariates included age, sex, education, deep and periventricular white matter hyperintensities, intracranial volume, hypertension, diabetes mellitus, and hyperlipidemia.

Results: BF volume mediated the association between FBB-SUVR and CTh both in AD and LBD spectra, while FBB-SUVR was associated with CTh independently of BF volume only in LBD spectrum. Significant correlation between voxel-wise FBB-SUVR and CTh was observed only in LBD group. FBB-SUVR was independently associated with widespread cognitive dysfunction both in AD and LBD spectra, especially in the memory domain [standardized beta (B) for AD spectrum = -0.60, B for LBD spectrum = -0.33]. In AD spectrum, BF volume was associated with memory dysfunction (B = 0.18), and CTh was associated with language (B = 0.21) and executive (B = 0.23) dysfunction. In LBD spectrum, however, BF volume and CTh were independently associated with widespread cognitive dysfunction.

Conclusions: There is a common β-amyloid-related degenerative mechanism with or without the mediation of BF in AD and LBD spectra, while the association of BF atrophy with cognitive dysfunction is more profound and there is localized β-amyloid-cortical atrophy interaction in LBD spectrum.

논문정보

형식Research article
게재일2021년 12월 (BRIC 등록일 2022-02-07)
연구진국내(교신)+국외 연구진
분야 의약학 > 응용의학

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