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Blood Hemoglobin, in-vivo Alzheimer Pathologies, and Cognitive Impairment: A Cross-Sectional Study

Authors
  • Kim, Jee Wook1, 2
  • Byun, Min Soo3
  • Yi, Dahyun4
  • Lee, Jun Ho5
  • Jeon, So Yeon6
  • Ko, Kang5
  • Joung, Haejung7
  • Jung, Gijung7
  • Lee, Jun-Young8
  • Sohn, Chul-Ho9
  • Lee, Yun-Sang10
  • Kim, Yu Kyeong11
  • Lee, Dong Young3, 7, 12
  • 1 Department of Neuropsychiatry, Hallym University Dongtan Sacred Heart Hospital, Hwaseong
  • 2 Department of Psychiatry, Hallym University College of Medicine, Chuncheon
  • 3 Department of Neuropsychiatry, Seoul National University Bundang Hospital, Seongnam
  • 4 Institute of Human Behavioral Medicine, Medical Research Center Seoul National University, Seoul
  • 5 Department of Geriatric Psychiatry, National Center for Mental Health, Seoul
  • 6 Department of Psychiatry, Chungnam National University Hospital, Daejeon
  • 7 Department of Neuropsychiatry, Seoul National University Hospital, Seoul
  • 8 Department of Neuropsychiatry, Seoul Metropolitan Government - Seoul National University Boramae Medical Center, Seoul
  • 9 Department of Radiology, Seoul National University Hospital, Seoul
  • 10 Department of Nuclear Medicine, Seoul National University College of Medicine, Seoul
  • 11 Department of Nuclear Medicine, Seoul Metropolitan Government - Seoul National University Boramae Medical Center, Seoul
  • 12 Department of Psychiatry, Seoul National University College of Medicine, Seoul
Type
Published Article
Journal
Frontiers in Aging Neuroscience
Publisher
Frontiers Media SA
Publication Date
Feb 24, 2021
Volume
13
Identifiers
DOI: 10.3389/fnagi.2021.625511
PMCID: PMC7943867
Source
PubMed Central
Keywords
License
Unknown

Abstract

Background: Despite known associations between low blood hemoglobin level and Alzheimer's disease (AD) or cognitive impairment, the underlying neuropathological links are poorly understood. We aimed to examine the relationships of blood hemoglobin levels with in vivo AD pathologies (i.e., cerebral beta-amyloid [Aβ] deposition, tau deposition, and AD-signature degeneration) and white matter hyperintensities (WMHs), which are a measure of cerebrovascular injury. We also investigated the association between hemoglobin level and cognitive performance, and then assessed whether such an association is mediated by brain pathologies. Methods: A total of 428 non-demented older adults underwent comprehensive clinical assessments, hemoglobin level measurement, and multimodal brain imaging, including Pittsburgh compound B-positron emission tomography (PET), AV-1451 PET, fluorodeoxyglucose (FDG)-PET, and magnetic resonance imaging. Episodic memory score and global cognition scores were also measured. Results: A lower hemoglobin level was significantly associated with reduced AD-signature cerebral glucose metabolism (AD-CM), but not Aβ deposition, tau deposition, or WMH volume. A lower hemoglobin level was also significantly associated with poorer episodic memory and global cognition scores, but such associations disappeared when AD-CM was controlled as a covariate, indicating that AD-CM has a moderating effect. Conclusion: The present findings suggest that low blood hemoglobin in older adults is associated with cognitive decline via reduced brain metabolism, which seems to be independent of those aspects of AD-specific protein pathologies and cerebrovascular injury that are reflected in PET and MRI measures.

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