Development of a Specific Diagnostic Test for Measurement of β-Amyloid (1-42) [βA4(l-42)] in CSF

Vanderstichele, Hugo; Blennow, Kaj; D’Heuvaert, N.; Buyse, Marie-Ange; Wallin, Anders; Andreasen, Niels; Seubert, Peter; Voorde, A. Van de; Vanmechelen, Eugeen

doi:10.1007/978-1-4615-5337-3_110

Cited by 55 publications

(56 citation statements)

References 9 publications

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“…A moderate to marked decrease in CSF A␤42 in AD to about 50% of control levels has been found using the majority of these methods (Table 1). 35,39,[41][42][43][44][45]47,48 An increase in CSF A␤42 in AD was found in one study. 46 This finding may be attributable to methodological differences (e.g., assay specificity for aggregated or truncated A␤ variants).…”

Section: ␤-Amyloidmentioning

confidence: 99%

“…There are 16 studies 41,49 -52,67,68,72,74,76,89,94,95,97-99 on the diagnostic performance of the most commonly used ELISA method 41 for A␤42 in CSF (Table 4). These studies include more than 650 AD patients and 500 controls (Table 4).…”

Section: A␤42mentioning

confidence: 99%

“…For the most commonly used ELISA methods for T-tau 14 and A␤42, 41 sensitivity and specificity figures are available from 12 studies (Table 5). 41,43,50,52,67,72,74,97,99 -102 The sensitivity and specificity for the combination of CSF T-tau and Ab42 have been slightly higher (89% and 90%, respectively) than for T-tau (81% and 91%, respectively) or Ab42 (86% and 89%, respectively) alone (Tables 2, 4, and 5).…”

Section: Combination Of Csf Biomarkers For Admentioning

confidence: 99%

“…61 The 20 largest studies 14,20,24,41,50,56,[62][63][64][65][66][67][68][69][70][71][72][73][74][75] including more than 2000 AD patients and 1000 controls, evaluating the most commonly used ELISA method for T-tau in CSF, 14 are summarized in Table 2. The mean sensitivity to discriminate AD from nondemented aged individuals has been 81%, at a specificity level of 91% (Table 2).…”

Section: Csf T-taumentioning

confidence: 99%

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Cerebrospinal fluid protein biomarkers for Alzheimer’s disease

2004

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Summary:The introduction of acetylcholine esterase (AChE) inhibitors as a symptomatic treatment of Alzheimer's disease (AD) has made patients seek medical advice at an earlier stage of the disease. This has highlighted the importance of diagnostic markers for early AD. However, there is no clinical method to determine which of the patients with mild cognitive impairment (MCI) will progress to AD with dementia, and which have a benign form of MCI without progression. In this paper, the performance of cerebrospinal fluid (CSF) protein biomarkers for AD is reviewed. The diagnostic performance of the three biomarkers, total tau, phospho-tau, and the 42 amino acid form of ␤-amyloid have been evaluated in numerous studies and their ability to identify incipient AD in MCI cases has also been studied. Some candidate AD biomarkers including ubiquitin, neurofilament proteins, growth-associated protein 43 (neuromodulin), and neuronal thread protein (AD7c) show interesting results but have been less extensively studied. It is concluded that CSF biomarkers may have clinical utility in the differentiation between AD and several important differential diagnoses, including normal aging, depression, alcohol dementia, and Parkinson's disease, and also in the identification of Creutzfeldt-Jakob disease in cases with rapidly progressive dementia. Early diagnosis of AD is not only of importance to be able to initiate symptomatic treatment with AChE inhibitors, but will be the basis for initiation of treatment with drugs aimed at slowing down or arresting the degenerative process, such as ␥-secretase inhibitors, if these prove to affect AD pathology and to have a clinical effect.

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Section: ␤-Amyloidmentioning

confidence: 99%

Section: A␤42mentioning

confidence: 99%

Section: Combination Of Csf Biomarkers For Admentioning

confidence: 99%

Section: Csf T-taumentioning

confidence: 99%

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Cerebrospinal fluid protein biomarkers for Alzheimer’s disease

2004

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“…This is exemplified by the finding that variants of the gene encoding apolipoprotein E (APOE) modify lipid levels (Yue et al 2005;Viiri et al 2005), which in turn contributes to Alzheimer's disease (AD OMIM 104300) and cardiovascular disease (CVD) (Corder et al 1993;Poirier et al 1993;Strittmatter et al 1993;Eichner et al 2002). As well as directly impacting plasma lipid levels, APOE also strongly affects b-amyloid (Ab) deposition in the brain (Beffert et al 1999), suggesting a connection between Ab, the main component of plaques, and apolipoprotein metabolism.…”

Section: Introductionmentioning

confidence: 99%

Quantitative trait loci in ABCA1 modify cerebrospinal fluid amyloid-β1-42 and plasma apolipoprotein levels

Katzov

Bennet

Höglund³

et al. 2005

J Hum Genet

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The ATP-binding cassette transporter A1 encoded by ABCA1 plays an integral role in the efflux of cellular cholesterol and phospholipids, but may also be a central mediator of b-amyloid (Ab) processing. Here, genetic association of the common R219K variant of ABCA1 is shown with cerebrospinal fluid (CSF) Ab 1-42 levels, reinforcing emerging evidence of a connection between lipid and Ab metabolism. In support of this finding we demonstrate for the first time that CSF cholesterol and Ab 1-42 are correlated. To affirm the plausible impact of ABCA1 variation on cholesterol and related traits as well as to empower a survey of possible interactions (e.g. age, gender, and smoking), a large Swedish population consisting of over 2,700 individuals was enlisted and extensive measures of plasma lipid parameters carried out. These analyses revealed that R219K has a strong effect on apolipoprotein B (APOB) and LDLcholesterol (LDL-C) among smokers (P=0.000055 and P=0.00059, respectively), but not among non-smokers. In contrast, no effect was evident with apolipoprotein A (APOA1) or HDL-cholesterol (HDL-C) levels. Plasma APOB and LDL-C, but not APOA1 and HDL-C, were shown to be markedly elevated in smokers versus nonsmokers, affirming that smoking may selectively impact the former pathway. No other genetic markers in ABCA1 exhibit effects as large as R219K, although a modest independent effect of R1587K was observed. Our data illuminate a possible genetic link between Ab and cholesterol metabolism, but also provide an intriguing example of an environmental exposure that may modify a genotype-phenotype relationship.

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Cerebrospinal Fluid β-Amyloid(1-42) in Alzheimer Disease

Andreasen¹,

Hesse²,

Davidsson³

et al. 1999

Arch Neurol

566

120

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The sensitivity of CSF-beta-amyloid(1-42) level as a diagnostic marker for AD is high. The intra-individual biological variation in CSF-beta-amyloid(1-42) level is low. Low CSF-beta-amyloid(1-42) levels are also found in the earlier stages of dementia in patients with AD. These findings suggest that CSF-beta-amyloid(1-42) analyses may be of value in the clinical diagnosis of AD, especially in the early course of the disease, when drug therapy may have the greatest potential of being effective but clinical diagnosis is particularly difficult.

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Development of a Specific Diagnostic Test for Measurement of β-Amyloid (1-42) [βA4(l-42)] in CSF

Cited by 55 publications

References 9 publications

Cerebrospinal fluid protein biomarkers for Alzheimer’s disease

Cerebrospinal fluid protein biomarkers for Alzheimer’s disease

Quantitative trait loci in ABCA1 modify cerebrospinal fluid amyloid-β1-42 and plasma apolipoprotein levels

Cerebrospinal Fluid β-Amyloid(1-42) in Alzheimer Disease

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