Effects of Lewy body disease and Alzheimer disease on brain atrophy and cognitive dysfunction

Sung Woo Kang, Seun Jeon, Han Soo Yoo, Seok Jong Chung, Phil Hyu Lee, Young H. Sohn, Mijin Yun, Alan C. Evans, Byoung Seok Ye

Research output: Contribution to journalArticlepeer-review

8 Citations (Scopus)

Abstract

ObjectivesTo investigate the independent and interaction effects of Alzheimer disease (AD) and Lewy body disease (LBD) on cognition and brain atrophy.MethodsWe consecutively recruited 38 controls and 108 patients with AD-related cognitive impairment (ADCI) and/or LBD-related cognitive impairment (LBCI) from university-based dementia and movement clinics. Diagnoses of ADCI and LBCI were supported by 18F-florbetaben PET and 18F-N-(3-fluoropropyl)-2β-carbon ethoxy-3β-(4-iodophenyl) nortropane-PET, respectively. There were 38 controls, 26 patients with pure ADCI (18 mild cognitive impairment [MCI] and 8 dementia), 28 patients with pure LBCI (13 MCI and 15 dementia), and 54 patients with mixed ADCI and LBCI (17 MCI and 37 dementia). We performed group-wise comparisons for neuropsychological z scores and regional cortical thickness. We also evaluated the effects of ADCI and LBCI using general linear models.ResultsCompared to the controls, patients in the pure ADCI group and pure LBCI group had focused cortical thinning in the bilateral entorhinal/right anterior temporal cortices and bilateral anteromedial temporal/basal frontal cortices, respectively, while the mixed disease group had additional cortical thinning in the widespread association cortices. The independent effects of ADCI and LBCI on regional cortical thinning overlapped in the widespread association cortices, especially at the bilateral temporoparietal junction and parietal cortices. ADCI and LBCI had independent detrimental effects on the copying item of the Rey-Osterrieth Complex Figure Test.ConclusionsConcomitant ADCI and LBCI are associated with the accentuation of neurodegeneration to widespread association cortices, and both diseases contribute to visuospatial dysfunction.

Original languageEnglish
Pages (from-to)E2015-E2026
JournalNeurology
Volume92
Issue number17
DOIs
Publication statusPublished - 2019 Apr 23

Bibliographical note

Funding Information:
This research was supported by a faculty research grant from Yonsei University College of Medicine (6-2018-0052), a National Research Foundation of Korea Grant funded by the Korean government (NRF-2016R1C1B1015044), and a grant from Canadian Institute of Health Research awarded to Professor Alan C. Evans (201085 and 247003). Dr. Seun Jeon is the recipient of following fellowships that contribute to his support: Bourse Fonds de Recherche Santé Québec (dossier 34240 and 259605) and the Jeanne Timmins Costello Fellowship of the Montreal Neurologic Institute (240522).

Funding Information:
This research was supported by a faculty research grant from Yonsei University College of Medicine (6-2018-0052), a National Research Foundation of Korea Grant funded by the Korean government (NRF- 2016R1C1B1015044), and a grant from Canadian Institute of Health Research awarded to Professor Alan C. Evans (201085 and 247003). Dr. Seun Jeon is the recipient of following fellowships that contribute to his support: Bourse Fonds de Recherche Sant? Qu?bec (dossier 34240 and 259605) and the Jeanne Timmins Costello Fellowship of the Montreal Neurologic Institute (240522).

Publisher Copyright:
© 2019 American Academy of Neurology.

All Science Journal Classification (ASJC) codes

  • Clinical Neurology

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