7
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Effect of apolipoprotein E phenotype on the association of plasma amyloid β and amyloid positron emission tomography imaging in Japan

      brief-report

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Introduction

          The plasma concentration of beta-amyloid (Aβ) has been considered another biomarker of Alzheimer's disease and was reportedly associated with cortical Aβ accumulation.

          Methods

          We analyzed 28 subjects with apolipoprotein E4 (ApoE4; E4 group) and 89 subjects without ApoE4 (non-E4 group) to determine the association between cortical Aβ accumulation by standard uptake value ratio with [ 18F]florbetapir positron emission tomography and plasma Aβ 1–40 and Aβ 1–42.

          Results

          1–42/Aβ 1–40 correlated significantly with mean regional [ 18F]florbetapir standard uptake value ratio in the non-E4 group ( R 2 = 0.06, P = .02) but not in the E4 group, and receiver operating characteristic curve analysis for Aβ 1–42/Aβ 1–40 in the non-E4 group showed sensitivity (92.9%) and specificity (45.9%) with a cutoff value of 0.150 for Aβ positivity.

          Discussion

          We verified that the correlation between Aβ 1–42/Aβ 1–40 and Aβ accumulation differed according to ApoE phenotype. The high sensitivity of plasma Aβ 1–42/Aβ 1–40 for Aβ positivity in non-E4 subjects indicated a possible role of plasma Aβ 1–42/Aβ 1–40 as a screening biomarker before amyloid positron emission tomography in clinical settings.

          Related collections

          Most cited references10

          • Record: found
          • Abstract: found
          • Article: not found

          A blood-based predictor for neocortical Aβ burden in Alzheimer's disease: results from the AIBL study.

          Dementia is a global epidemic with Alzheimer's disease (AD) being the leading cause. Early identification of patients at risk of developing AD is now becoming an international priority. Neocortical Aβ (extracellular β-amyloid) burden (NAB), as assessed by positron emission tomography (PET), represents one such marker for early identification. These scans are expensive and are not widely available, thus, there is a need for cheaper and more widely accessible alternatives. Addressing this need, a blood biomarker-based signature having efficacy for the prediction of NAB and which can be easily adapted for population screening is described. Blood data (176 analytes measured in plasma) and Pittsburgh Compound B (PiB)-PET measurements from 273 participants from the Australian Imaging, Biomarkers and Lifestyle (AIBL) study were utilised. Univariate analysis was conducted to assess the difference of plasma measures between high and low NAB groups, and cross-validated machine-learning models were generated for predicting NAB. These models were applied to 817 non-imaged AIBL subjects and 82 subjects from the Alzheimer's Disease Neuroimaging Initiative (ADNI) for validation. Five analytes showed significant difference between subjects with high compared to low NAB. A machine-learning model (based on nine markers) achieved sensitivity and specificity of 80 and 82%, respectively, for predicting NAB. Validation using the ADNI cohort yielded similar results (sensitivity 79% and specificity 76%). These results show that a panel of blood-based biomarkers is able to accurately predict NAB, supporting the hypothesis for a relationship between a blood-based signature and Aβ accumulation, therefore, providing a platform for developing a population-based screen.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Changes in plasma amyloid beta in a longitudinal study of aging and Alzheimer's disease.

            A practical biomarker is required to facilitate the preclinical diagnosis of Alzheimer's disease (AD). Plasma amyloid beta (Aβ)1-40, Aβ1-42, Aβn-40, and Aβn-42 peptides were measured at baseline and after 18 months in 771 participants from the Australian Imaging Biomarkers and Lifestyle (AIBL) study of aging. Aβ peptide levels were compared with clinical pathology, neuroimaging and neuropsychological measurements. Although inflammatory and renal function covariates influenced plasma Aβ levels significantly, a decrease in Aβ1-42/Aβ1-40 was observed in patients with AD, and was also inversely correlated with neocortical amyloid burden. During the 18 months, plasma Aβ1-42 decreased in subjects with mild cognitive impairment (MCI) and in those transitioning from healthy to MCI. Our findings are consistent with a number of published plasma Aβ studies and, although the prognostic value of individual measures in any given subject is limited, the diagnostic contribution of plasma Aβ may demonstrate utility when combined with a panel of peripheral biomarkers. Crown Copyright © 2014. Published by Elsevier Inc. All rights reserved.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Meta-analysis of plasma amyloid-β levels in Alzheimer's disease.

              Plasma amyloid-β (Aβ) levels have been proposed as biomarkers of Alzheimer's disease (AD), but studies have produced inconsistent results. We present a meta-analytic review of cross-sectional studies that examined plasma Aβ levels in AD and cognitively normal subjects, and longitudinal studies that used baseline plasma Aβ levels to predict conversion from normal cognition to AD. Medline and EMBASE databases were searched to generate an initial list of relevant studies, and selected authors approached for additional data. Twelve cross- sectional studies (n = 1483) and seven longitudinal (n = 3920) met the inclusion criteria for meta-analysis. Random effects model was used to calculate the weighted mean difference (WMD) by Review Manager Version 4.2. In longitudinal studies, cognitively normal individuals who converted to AD had higher baseline Aβ1-40 and Aβ1-42 levels (WMD: 10.29, z = 3.80, p = 0.0001 and WMD: 8.01, z = 2.76, p = 0.006, respectively), and non-significantly increased Aβ1-42/Aβ1-40 ratio (WMD: 0.03, z = 1.65, p = 0.10). In cross sectional studies, compared to cognitively normal individuals, AD patients had marginally but non-significantly lower Aβ1-42 levels (WMD:-2.84, z = 1.73, p = 0.08), but Aβ1-40 levels were not significantly different (WMD: 3.43, z = 0.40, p = 0.69). Our systematic review suggests a model of differential longitudinal changes in plasma Aβ levels in cognitively stable individuals versus those who go on to develop AD dementia. Baseline Aβ1-40 and Aβ1-42 levels in cognitively normal elderly individuals might be predictors of higher rates of progression to AD, and should be further explored as potential biomarkers.
                Bookmark

                Author and article information

                Contributors
                Journal
                Alzheimers Dement (Amst)
                Alzheimers Dement (Amst)
                Alzheimer's & Dementia : Diagnosis, Assessment & Disease Monitoring
                Elsevier
                2352-8729
                05 September 2017
                2017
                05 September 2017
                : 9
                : 51-56
                Affiliations
                [a ]Department of Neuropsychiatry, Nippon Medical School, Bunkyo-ku, Tokyo, Japan
                [b ]Department of Radiology, Nippon Medical School, Bunkyo-ku, Tokyo, Japan
                [c ]Department of Pharmacology, Nippon Medical School, Bunkyo-ku, Tokyo, Japan
                Author notes
                []Corresponding author. Tel.: +81-3-3822-2131; Fax: +81-3-5814-6287. okubo-y@ 123456nms.ac.jp
                Article
                S2352-8729(17)30049-0
                10.1016/j.dadm.2017.08.002
                5614760
                5ecf197c-b8c1-4ba9-817c-a195f2e65d68
                © 2017 The Authors

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                Categories
                Neuroimaging

                alzheimer's disease,plasma beta-amyloid1–40,plasma beta-amyloid1–42,beta-amyloid1–40/beta-amyloid1–42,positron emission tomography,phenotype of apolipoprotein

                Comments

                Comment on this article