An Alzheimer's disease-specific β-amyloid fragment signature in cerebrospinal fluid

Portelius, Erik; Zetterberg, Henrik; Andréasson, Ulf; Brinkmalm, Gunnar; Andreasen, Niels; Wallin, Anders; Westman‐Brinkmalm, Ann; Blennow, Kaj

doi:10.1016/j.neulet.2006.09.044

Cited by 116 publications

(84 citation statements)

References 22 publications

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“…An increase in CSF Ab1 -16 is found in AD together with the expected decrease in Ab1-42 (Portelius et al 2006b(Portelius et al , 2010. Data from experimental studies show that the shorter Ab isoforms Ab1-14, Ab1 -15, and Ab1 -16 are produced by a novel pathway for APP processing involving the concerted action of b-and a-secretase, whereas the longer isoforms, from Ab1-17 and up to Ab1-42, are produced in the g-secretase pathway (Portelius et al 2009).…”

Section: Fluid Biomarkers In Alzheimer Diseasementioning

confidence: 82%

Fluid Biomarkers in Alzheimer Disease

Blennow

Zetterberg

Fagan

2012

Cold Spring Harbor Perspectives in Medicine

167

148

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Research progress has provided detailed understanding of the molecular pathogenesis of Alzheimer disease (AD). This knowledge has been translated into new drug candidates with putative disease-modifying effects, which are now being tested in clinical trials. The promise of effective therapy has created a great need for biomarkers able to detect AD in the predementia phase, because drugs will probably be effective only if neurodegeneration is not too advanced. In this chapter, cerebrospinal fluid (CSF) and plasma biomarkers are reviewed. The core CSF biomarkers total tau (T-tau), phosphorylated tau (P-tau) and the 42 amino acid form of b-amyloid (Ab42) reflect AD pathology, and have high diagnostic accuracy to diagnose AD with dementia and prodromal AD in mild cognitive impairment cases. The rationale for the use of CSF biomarkers to identify and monitor the mechanism of action of new drug candidates is also outlined in this chapter.

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Section: Fluid Biomarkers In Alzheimer Diseasementioning

confidence: 82%

Fluid Biomarkers in Alzheimer Disease

Blennow

Zetterberg

Fagan

2012

Cold Spring Harbor Perspectives in Medicine

167

148

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“…Part of research concentrates on identification of novel Aß truncated forms that could allow better predictive power and specificity of biological diagnosis (Bibl, Mollenhauer et al 2007). Indeed, new Aß 13 , Aß 14 or else Aß 16 peptides were described within CSF of AD patients and surprisingly Aß 16 CSF levels increase in AD patients (Portelius, Zetterberg et al 2006). Identification of these Aß fragments in the CSF could lead to a more specific differential diagnosis since it may exist distinct CSF Aß fragment profiles between AD, DLB or FTD, these profiles could reflect distinct physiopathological events between these pathologies (Bibl, Mollenhauer et al 2007).…”

Section: Which Csf Biochemical Markers Might Allow Us To Detect Alzhementioning

confidence: 99%

Alzheimer’s Diseases: Towards Biomarkers for an Early Diagnosis

Elmoualij¹,

Dupiereux-Fettweis²,

Seguin³

et al. 2011

The Clinical Spectrum of Alzheimer's Disease -the Charge Toward Comprehensive Diagnostic and Therapeutic Strategies

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“…For example, mass spectrometric profiling of A␤ catabolites in cerebrospinal fluid has been reported to distinguish AD patients from age-matched controls with high selectivity and specificity (47). Another promising line of research is the development of methods to monitor A␤ catabolism in real time in humans (48).…”

Section: Categories Of Investigationmentioning

confidence: 99%

The AβCs of Aβ-cleaving Proteases

Leissring

2008

Journal of Biological Chemistry

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The amyloid ␤-protein (A␤), which accumulates abnormally in Alzheimer disease (AD), is degraded by a diverse set of proteolytic enzymes. A␤-cleaving proteases, largely ignored until only recently, are now known to play a pivotal role in the regulation of cerebral A␤ levels and amyloid plaque formation in animal models, and accumulating evidence suggests that defective A␤ proteolysis may be operative in many AD cases. This review summarizes the growing body of evidence supporting the involvement of specific A␤-cleaving proteases in the etiology and potential treatment of AD. Recognition of the importance of A␤ degradation to the overall economy of A␤ has revised our thinking about the mechanistic basis of AD pathogenesis and identified a novel class of enzymes that may serve as both therapeutic targets and therapeutic agents.

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An Alzheimer's disease-specific β-amyloid fragment signature in cerebrospinal fluid

Cited by 116 publications

References 22 publications

Fluid Biomarkers in Alzheimer Disease

Fluid Biomarkers in Alzheimer Disease

Alzheimer’s Diseases: Towards Biomarkers for an Early Diagnosis

The AβCs of Aβ-cleaving Proteases

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