期刊
NEUROBIOLOGY OF AGING
卷 36, 期 8, 页码 2340-2347出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.neurobiolaging.2015.04.011
关键词
Alzheimer's disease; Cerebrospinal fluid; Magnetic resonance imaging; Amyloid; Tau; Atrophy
资金
- Marie Curie FP7 International Outgoing Fellowship [628812]
- BrightFocus Foundation
- Alzheimer's Disease Research
- National Institute on Aging [R01-AG045611]
- John Douglas French Alzheimer's Foundation
- Alzheimer Nederland
- Stichting VUMC funds
- Stichting Dioraphte
- NATIONAL INSTITUTE ON AGING [P50AG023501, R01AG045611] Funding Source: NIH RePORTER
Different clinical variants of probable Alzheimer's disease (AD) share underlying plaques and tangles but show distinct atrophy patterns. We included 52 posterior cortical atrophy, 29 logopenic variant primary progressive aphasia, 53 early-onset and 42 late-onset AD patients, selected for abnormal cerebrospinal fluid (CSF) eamyloid-beta(42), with CSF and magnetic resonance imaging data available. Bootstrapping revealed no differences in the prevalence of abnormal CSF total-tau and phosphorylated-tau between probable AD variants (range total-tau: 84.9%-92.3%, phosphorylated-tau: 79.2%-93.1%, p > 0.05). Voxelwise linear regressions showed various relationships between lower CSF-A beta(42) and syndrome-specific atrophy, involving precuneus, posterior cingulate, and medial temporal lobe in early-onset AD, occipital cortex and middle temporal gyrus in posterior cortical atrophy; anterior cingulate, insular cortex and precentral gyrus (left > right) in logopenic variant primary progressive aphasia; and medial temporal lobe, thalamus, and temporal pole in late-onset AD (all at p < 0.001 uncorrected). In contrast, CSF-tau was not related to gray matter atrophy in any group. Our findings suggest that lower CSF eamyloid-beta(42) - and not increased total-tau and phosphorylated-tau - relates to reduced gray matter volumes, mostly in regions that are typically atrophied in distinct clinical variants of probable AD. (C) 2015 Elsevier Inc. All rights reserved.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据