Amyloid-β-related and unrelated cortical thinning in dementia with Lewy bodies

Young gun Lee; Seun Jeon; Han Soo Yoo; Seok Jong Chung; Seung Koo Lee; Phil Hyu Lee; Young Ho Sohn; Mijin Yun; Alan C. Evans; Byoung Seok Ye

doi:10.1016/j.neurobiolaging.2018.08.007

Amyloid-β-related and unrelated cortical thinning in dementia with Lewy bodies

Young gun Lee, Seun Jeon, Han Soo Yoo, Seok Jong Chung, Seung Koo Lee, Phil Hyu Lee, Young Ho Sohn, Mijin Yun, Alan C. Evans, Byoung Seok Ye

Department of Neurology

Research output: Contribution to journal › Article › peer-review

6 Citations (Scopus)

Abstract

Coexisting Alzheimer's disease (AD) pathology is common in patients with dementia with Lewy bodies (DLB). To evaluate the cortical thinning in patients with DLB considering the effect of amyloid-β (Aβ), we compared the regional cortical thickness between control subjects and patients with DLB with abnormal dopamine transporter imaging. Seventeen (43.6%) of 39 patients with DLB and no control subjects had significant Aβ deposition on ¹⁸F-florbetaben positron emission tomography. Compared to control (n = 15), Aβ-negative DLB group (n = 21) had cortical thinning in the bilateral insula, entorhinal, basal frontal, and occipito-parietal cortices. Compared to Aβ-negative DLB, Aβ-positive DLB group (n = 15) had a lower cortical thickness in the AD-prone brain regions in addition to the bilateral occipital, basal frontal, and somatomotor cortices. After controlling for the amount of Aβ deposition, DLB group had cortical thinning in the same regions affected in the Aβ-negative DLB group. In summary, patients with DLB had an Aβ-independent cortical thinning, while Aβ was associated with additional cortical thinning in the AD-prone brain regions and the aggravation of DLB-specific cortical thinning.

Original language	English
Pages (from-to)	32-39
Number of pages	8
Journal	Neurobiology of Aging
Volume	72
DOIs	https://doi.org/10.1016/j.neurobiolaging.2018.08.007
Publication status	Published - 2018 Dec

Bibliographical note

Funding Information:
This research was supported by a faculty research grant from Yonsei University College of Medicine (6-2016-0080), a grant from National Research Foundation of Korea Grant funded by the Korean Government (NRF-2016R1C1B1015044), and a grant from Canadian Institute of Health Research (CIHR) awarded to Professor Alan C. Evans (201085 and 247003). SJ is the recipient of following fellowships that contribute to his support: Bourse Fonds de Recherche Santé Québec (FRQS, dossier 34240 & 259605) and the Jeanne Timmins Costello Fellowship of the Montreal Neurological Institute (240522).

All Science Journal Classification (ASJC) codes

Neuroscience(all)
Ageing
Clinical Neurology
Developmental Biology
Geriatrics and Gerontology

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@article{a037cf0dab154c3eae293181f766504b,

title = "Amyloid-β-related and unrelated cortical thinning in dementia with Lewy bodies",

abstract = "Coexisting Alzheimer's disease (AD) pathology is common in patients with dementia with Lewy bodies (DLB). To evaluate the cortical thinning in patients with DLB considering the effect of amyloid-β (Aβ), we compared the regional cortical thickness between control subjects and patients with DLB with abnormal dopamine transporter imaging. Seventeen (43.6%) of 39 patients with DLB and no control subjects had significant Aβ deposition on 18F-florbetaben positron emission tomography. Compared to control (n = 15), Aβ-negative DLB group (n = 21) had cortical thinning in the bilateral insula, entorhinal, basal frontal, and occipito-parietal cortices. Compared to Aβ-negative DLB, Aβ-positive DLB group (n = 15) had a lower cortical thickness in the AD-prone brain regions in addition to the bilateral occipital, basal frontal, and somatomotor cortices. After controlling for the amount of Aβ deposition, DLB group had cortical thinning in the same regions affected in the Aβ-negative DLB group. In summary, patients with DLB had an Aβ-independent cortical thinning, while Aβ was associated with additional cortical thinning in the AD-prone brain regions and the aggravation of DLB-specific cortical thinning.",

author = "Lee, {Young gun} and Seun Jeon and Yoo, {Han Soo} and Chung, {Seok Jong} and Lee, {Seung Koo} and Lee, {Phil Hyu} and Sohn, {Young Ho} and Mijin Yun and Evans, {Alan C.} and Ye, {Byoung Seok}",

note = "Funding Information: This research was supported by a faculty research grant from Yonsei University College of Medicine (6-2016-0080), a grant from National Research Foundation of Korea Grant funded by the Korean Government (NRF-2016R1C1B1015044), and a grant from Canadian Institute of Health Research (CIHR) awarded to Professor Alan C. Evans (201085 and 247003). SJ is the recipient of following fellowships that contribute to his support: Bourse Fonds de Recherche Sant{\'e} Qu{\'e}bec (FRQS, dossier 34240 & 259605) and the Jeanne Timmins Costello Fellowship of the Montreal Neurological Institute (240522). ",

year = "2018",

month = dec,

doi = "10.1016/j.neurobiolaging.2018.08.007",

language = "English",

volume = "72",

pages = "32--39",

journal = "Neurobiology of Aging",

issn = "0197-4580",

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T1 - Amyloid-β-related and unrelated cortical thinning in dementia with Lewy bodies

AU - Lee, Young gun

AU - Jeon, Seun

AU - Yoo, Han Soo

AU - Chung, Seok Jong

AU - Lee, Seung Koo

AU - Lee, Phil Hyu

AU - Sohn, Young Ho

AU - Yun, Mijin

AU - Evans, Alan C.

AU - Ye, Byoung Seok

N1 - Funding Information: This research was supported by a faculty research grant from Yonsei University College of Medicine (6-2016-0080), a grant from National Research Foundation of Korea Grant funded by the Korean Government (NRF-2016R1C1B1015044), and a grant from Canadian Institute of Health Research (CIHR) awarded to Professor Alan C. Evans (201085 and 247003). SJ is the recipient of following fellowships that contribute to his support: Bourse Fonds de Recherche Santé Québec (FRQS, dossier 34240 & 259605) and the Jeanne Timmins Costello Fellowship of the Montreal Neurological Institute (240522).

PY - 2018/12

Y1 - 2018/12

N2 - Coexisting Alzheimer's disease (AD) pathology is common in patients with dementia with Lewy bodies (DLB). To evaluate the cortical thinning in patients with DLB considering the effect of amyloid-β (Aβ), we compared the regional cortical thickness between control subjects and patients with DLB with abnormal dopamine transporter imaging. Seventeen (43.6%) of 39 patients with DLB and no control subjects had significant Aβ deposition on 18F-florbetaben positron emission tomography. Compared to control (n = 15), Aβ-negative DLB group (n = 21) had cortical thinning in the bilateral insula, entorhinal, basal frontal, and occipito-parietal cortices. Compared to Aβ-negative DLB, Aβ-positive DLB group (n = 15) had a lower cortical thickness in the AD-prone brain regions in addition to the bilateral occipital, basal frontal, and somatomotor cortices. After controlling for the amount of Aβ deposition, DLB group had cortical thinning in the same regions affected in the Aβ-negative DLB group. In summary, patients with DLB had an Aβ-independent cortical thinning, while Aβ was associated with additional cortical thinning in the AD-prone brain regions and the aggravation of DLB-specific cortical thinning.

AB - Coexisting Alzheimer's disease (AD) pathology is common in patients with dementia with Lewy bodies (DLB). To evaluate the cortical thinning in patients with DLB considering the effect of amyloid-β (Aβ), we compared the regional cortical thickness between control subjects and patients with DLB with abnormal dopamine transporter imaging. Seventeen (43.6%) of 39 patients with DLB and no control subjects had significant Aβ deposition on 18F-florbetaben positron emission tomography. Compared to control (n = 15), Aβ-negative DLB group (n = 21) had cortical thinning in the bilateral insula, entorhinal, basal frontal, and occipito-parietal cortices. Compared to Aβ-negative DLB, Aβ-positive DLB group (n = 15) had a lower cortical thickness in the AD-prone brain regions in addition to the bilateral occipital, basal frontal, and somatomotor cortices. After controlling for the amount of Aβ deposition, DLB group had cortical thinning in the same regions affected in the Aβ-negative DLB group. In summary, patients with DLB had an Aβ-independent cortical thinning, while Aβ was associated with additional cortical thinning in the AD-prone brain regions and the aggravation of DLB-specific cortical thinning.

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