Amyloid-Independent Amnestic Mild Cognitive Impairment and Serum Apolipoprotein A1 Levels
- Authors
- Choi, Hyo Jung; Seo, Eun Hyun; Yi, Dahyun; Sohn, Bo Kyung; Choe, Young Min; Byun, Min Soo; Lee, Jong Min; Woo, Jong Inn; Lee, Dong Young
- Issue Date
- Feb-2016
- Publisher
- ELSEVIER SCIENCE INC
- Keywords
- Amyloid PET; MRI; mild cognitive impairment; Alzheimer disease; apolipoprotein
- Citation
- AMERICAN JOURNAL OF GERIATRIC PSYCHIATRY, v.24, no.2, pp.144 - 153
- Indexed
- SCIE
SSCI
SCOPUS
- Journal Title
- AMERICAN JOURNAL OF GERIATRIC PSYCHIATRY
- Volume
- 24
- Number
- 2
- Start Page
- 144
- End Page
- 153
- URI
- https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/155164
- DOI
- 10.1016/j.jagp.2015.06.004
- ISSN
- 1064-7481
- Abstract
- Objectives: The present study investigated the characteristics of amnestic mild cognitive impairment (aMCI) in subjects with low brain amyloid-beta (Ab) burden. Furthermore, the relationships between amyloid-independent cognitive decline and serum lipid profiles, particularly apolipoprotein A1 (APOA1), were evaluated. Design: Cross-sectional and longitudinal follow-up study. Setting: University hospital dementia clinic. Participants: 28 aMCI and 35 cognitive normal (CN) elderly. Measurements: The study measures included baseline assessments of the subjects' clinical characteristics, lipid profiles, and magnetic resonance imaging and C-11-labelled Pittsburgh Compound B (PiB) positron emission tomography scans. Based on PiB retention at baseline, the aMCI subjects were divided into low A beta (aMCI-) and high A beta (aMCI+) subgroups. All aMCI subjects were followed up over a 1-year period. Results: The aMCI- group had a longer duration of illness than did the aMCI \ group. None of the aMCI subjects were diagnosed with Alzheimer disease (AD) dementia during the 1-year follow-up period, whereas 26.7% of aMCI+ subjects developed AD dementia. The aMCI- group also exhibited lower serum APOA1 levels compared with both the aMCI+ and CN groups. Additionally, lower serum APOA1 levels were associated with cognitive decline and brain atrophy independent of A beta deposition and vascular burden. Conclusions: Patients with aMCI- likely exhibit different clinical and pathophysiological characteristics than patients with aMCI+. Additionally, APOA1 may be an important contributor underlying amyloid-independent neurodegeneration.
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