Cerebrospinal fluid neuronal pentraxin receptor as a biomarker of long-term progression of Alzheimer's disease: a 24-month follow-up study

被引:21
|
作者
Lim, Bryant [1 ]
Sando, Sigrid Botne [2 ,3 ]
Grontvedt, Goril Rolfseng [2 ,3 ]
Brathen, Geir [2 ,3 ]
Diamandis, Eleftherios P. [1 ,4 ,5 ]
机构
[1] Univ Toronto, Dept Lab Med & Pathobiol, Toronto, ON, Canada
[2] Univ Hosp Trondheim, Dept Neurol & Clin Neurophysiol, Trondheim, Norway
[3] Norwegian Univ Sci & Technol NTNU, Dept Neuromed & Movement Sci, Trondheim, Norway
[4] Mt Sinai Hosp, Dept Pathol & Lab Med, Toronto, ON, Canada
[5] Univ Hlth Network, Dept Clin Biochem, Toronto, ON, Canada
关键词
Alzheimer's disease; Cerebrospinal fluid; Neuronal pentraxin receptor; Biomarker; Progression; Longitudinal study; MILD COGNITIVE IMPAIRMENT; CSF BIOMARKERS; RECOMMENDATIONS; ACTIVATION; DEMENTIA;
D O I
10.1016/j.neurobiolaging.2020.03.013
中图分类号
R592 [老年病学]; C [社会科学总论];
学科分类号
03 ; 0303 ; 100203 ;
摘要
Lower cerebrospinal fluid (CSF) levels of neuronal pentraxin receptor (NPTXR) are associated with Alzheimer's disease (AD), but few studies show longitudinal changes in CSF NPTXR. In the present study, CSF NPTXR was measured at 0, 12, and 24 months using an enzyme-linked immunosorbent assay. The study groups included 28 patients with mild cognitive impairment (MCI) (MCI-MCI), 27 MCI patients who progressed to AD (MCI-AD) during the study, and 28 AD patients (AD-AD). Baseline levels were assessed for 46 control individuals. AD patients had lower baseline CSF NPTXR than controls (p = 0.023). Linear mixed models estimated a 6.7% annualized decrease in CSF NPTXR in the AD-AD group, significantly different from MCI-MCI (p = 0.03) and MCI-AD groups (p = 0.048). CSF NPTXR did not correlate with CSF A beta 42 and weakly correlated with CSF A beta 40, T-tau, P-tau (all R-2 < 0.22, p < 0.06). These trends suggest CSF NPTXR may be a candidate biomarker of AD progression but not sufficiently sensitive to resolve when patients convert from MCI to dementia. (C) 2020 Elsevier Inc. All rights reserved.
引用
收藏
页码:97.e1 / 97.e7
页数:7
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