Amyloid β protein in plasma from patients with sporadic Alzheimer's disease

Tamaoka, Akira; Fukushima, Tetsuo; Sawamura, Naoya; Ishikawa, Kinya; Oguni, Eiichi; Komatsuzaki, Yoshimasa; Shoji, Shin’ichi

doi:10.1016/0022-510x(96)00143-8

Cited by 147 publications

(103 citation statements)

References 22 publications

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“…It is also possible the presence of high intra-and inter-person variability due to factors that could influence the levels of a potential biomarker. The majority of the efforts in finding plasma biomarkers for neurodegenerative disorders have been made in AD, starting more than a decade ago with the traditional approach of measuring one molecule closely related to the pathology of the disease, in this case beta-amyloid (Aβ) (Mayeux et al, 1999;Tamaoka et al, 1996;Vanderstichele et al, 2000).…”

Section: Biomarkers In Plasmamentioning

confidence: 99%

“…Plasma total Aβ or Aβ-42 are increased in cases of familial AD (Kosaka et al, 1997;Scheuner et al, 1996) and in Downs syndrome with amyloid precursor protein (APP) triplication (Schupf et al, 2001) but the results were not consistent with the diagnosis of sporadic AD (Assini et al, 2004;Fukumoto et al, 2003;Mayeux et al, 1999;Schupf et al, 2001;Tamaoka et al, 1996;Vanderstichele et al, 2000). Peripheral Aβ is transported via receptor for advanced glycation end products (RAGE) across the BBB into the brain (Deane et al, 2004) and Aβ elimination from brain across the BBB by cell surface low-density lipoprotein receptor related protein-1 (LRP) (Sagare et al, 2007).…”

Section: Biomarkers In Plasmamentioning

confidence: 99%

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Biomarkers for Alzheimer’s disease and other forms of dementia: Clinical needs, limitations and future aspects

Cedazo-Minguez

Winblad

2010

Experimental Gerontology

136

133

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To cite this version:Angel Cedazo-Minguez, Bengt Winblad. Biomarkers for Alzheimer's disease and other forms of dementia: clinical needs, limitations and future aspects. Experimental Gerontology, Elsevier, 2009, 45 (1), pp. This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. ACCEPTED MANUSCRIPT

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Section: Biomarkers In Plasmamentioning

confidence: 99%

Section: Biomarkers In Plasmamentioning

confidence: 99%

Biomarkers for Alzheimer’s disease and other forms of dementia: Clinical needs, limitations and future aspects

Cedazo-Minguez

Winblad

2010

Experimental Gerontology

136

133

View full text Add to dashboard Cite

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“…BACE cleaves APP and releases a large N-terminal fragment (sAPPβ). The membrane-anchored frag- [73,75] Decreased [65] β-amyloid (Aβ) Decreased [45,46] No difference [79][80][81][82] No difference [47] Aβ1- 40 No difference [24] No difference [83] Increased [84] Decreased [85] Aβ1- 42 Decreased [24] Increased [83] -Aβ1-42/Aβ1-40 ratio Decreased [48] No difference [83] Decreased [78,84,86] APP ratio --Decreased [90][91][92][93] Ubiquitin Increased [24] No difference [148] BACE1 Increased [67] --Cholesterol -Decreased [94,95] Increased [96][97][98] 24S-hydroxycholesterol Increased [102] No difference [103] Decreased [104] Homocysteine -Increased [106,107,109] Epidermal growth factor -Decreased [111] Decreased [93] Increased [112] Glial cell line-derived growth factor -Decreased [111] No difference …”

Section: Aβ1-42mentioning

confidence: 99%

“…In familial AD cases, total Aβ and Aβ1-42 plasma levels are elevated [79] . In sporadic AD, several cross-sectional studies report no significant difference in plasma Aβ concentrations in general compared to controls [79][80][81][82] . Unfortunately, longitudinal studies have shown high data variability.…”

Section: Aβ Peptidesmentioning

confidence: 99%

Cerebrospinal fluid and blood biomarkers in Alzheimer’s disease

Humpel

Hochstrasser²

2011

WJP

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Due to an ever aging society and growing prevalence of Alzheimer's disease (AD), the challenge to meet social and health care system needs will become increasingly difficult. Unfortunately, a definite ante mortem diagnosis is not possible. Thus, an early diagnosis and identification of AD patients is critical for promising, early pharmacological interventions as well as addressing health care needs. The most advanced and most reliable markers are β-amyloid, total tau and phosphorylated tau in cerebrospinal fluid (CSF). In blood, no single biomarker has been identified despite an intense search over the last decade. The most promising approaches consist of a combination of several bloodbased markers increasing the reliability, sensitivity and specificity of the AD diagnosis. However, contradictory data make standardized testing methods in longitudinal and multi-center studies extremely difficult. In this review, we summarize a range of the most promising CSF and blood biomarkers for diagnosing AD.

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“…Lönneborg [21] summarized in 2008 that of several studies that investigated plasma A␤ levels in AD; one study showed an increase in A␤ levels [25] and the majority of studies found no significant differences between AD and controls [26][27][28][29][30]. Later, a systematic review and meta-analysis in 2012 by Koyama et al [31] concluded that plasma A␤ 42 :A␤ 40 ratio may predict development of AD, however, significant heterogeneity in the meta-analysis underlines the need for substantial further investigation of plasma A␤ levels as a preclinical biomarker.…”

Section: Introductionmentioning

confidence: 99%

Prediction of Mild Cognitive Impairment that Evolves into Alzheimer's Disease Dementia within Two Years using a Gene Expression Signature in Blood: A Pilot Study

Roed

Grave

Lindahl

et al. 2013

JAD

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Background: The focus on Alzheimer's disease (AD) is shifting from dementia to the prodromal stage of the disorder, to a large extent due to increasing efforts in trying to develop disease modifying treatment for the disorder. For development of diseasemodifying drugs, a reliable and accurate test for identification of mild cognitive impairment (MCI) due to AD is essential. Objective: In the present study, MCI progressing to AD will be predicted using blood-based gene expression. Material and Methods: Gene expression analysis using qPCR was performed on blood RNA from a cohort of patients with amnestic MCI (aMCI; n = 66). Within the aMCI cohort, patients progressing to AD within 1 to 2 years were grouped as MCI converters (n = 34) and the patients remaining at the MCI stage after 2 years were grouped as stable MCI (n = 32). AD and control populations were also included in the study. Results: Multivariate statistical method partial least square regression was used to develop predictive models which later were tested using leave-one-out cross validation. Gene expression signatures that identified aMCI subjects that progressed to AD within 2 years with a prediction accuracy of 74%-77% were identified for the complete dataset and subsets thereof. Conclusion:The present pilot study demonstrates for the first time that MCI that evolves into AD dementia within 2 years may be predicted by analyzing gene expression in blood. Further studies will be needed to validate this gene signature as a potential test for AD in the predementia stage.

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Amyloid β protein in plasma from patients with sporadic Alzheimer's disease

Cited by 147 publications

References 22 publications

Biomarkers for Alzheimer’s disease and other forms of dementia: Clinical needs, limitations and future aspects

Biomarkers for Alzheimer’s disease and other forms of dementia: Clinical needs, limitations and future aspects

Cerebrospinal fluid and blood biomarkers in Alzheimer’s disease

Prediction of Mild Cognitive Impairment that Evolves into Alzheimer's Disease Dementia within Two Years using a Gene Expression Signature in Blood: A Pilot Study

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