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Cortical Thinning in Subcortical Vascular Dementia with Negative C-11-PiB PET

Authors
Kim, Chi HunSeo, Sang WonKim, Geon HaShin, Ji SooCho, HannaNoh, YoungKim, Suk-HuiKim, Min JiJeon, SeunYoon, UicheulLee, Jong-MinOh, Seung JunKim, Jae SeungKim, Sung TaeLee, Jae-HongNa, Duk L.
Issue Date
Jul-2012
Publisher
IOS Press
Keywords
Alzheimer' s disease; cortical thickness; Pittsburgh compound B; subcortical vascular dementia
Citation
Journal of Alzheimer's Disease, v.31, no.2, pp.315 - 323
Indexed
SCIE
SCOPUS
Journal Title
Journal of Alzheimer's Disease
Volume
31
Number
2
Start Page
315
End Page
323
URI
https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/165126
DOI
10.3233/JAD-2012-111832
ISSN
1387-2877
Abstract
To determine the existence of cortical thinning in subcortical vascular dementia (SVaD) with a negative C-11-Pittsburgh compound B (PiB) positron emission tomography scan and to compare the topography of cortical thinning between PiB-negative SVaD and Alzheimer's disease (AD), we enrolled 24 patients with PiB(-) SVaD, 81 clinically probable AD individuals, and 72 normal cognitive controls. Compared with controls, cortical thinning in PiB(-) SVaD was most profound in the perisylvian area, medial prefrontal area, and posterior cingulate gyri, while the precuneus and medial temporal lobes were relatively spared. When the cortical thickness of AD and PiB(-) SVaD were directly compared, PiB(-) SVaD demonstrated significant cortical thinning in the bilateral inferior frontal, superior temporal gyri, and right medial frontal and orbitofrontal lobes, while AD showed significant cortical thinning in the right medial temporal region. SVaD without amyloid burden may lead to substantial cortical atrophy. Moreover, characteristic topography of cortical thinning in PiB(-) SVaD suggests different mechanisms of cortical thinning in PiB(-) SVaD and AD.
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