Abstract
Alzheimers disease (AD) is an age-related disorder that causes brain damage resulting in progressive cognitive impairment and death. Three decades of progress have given us a detailed understanding of the underlying molecular mechanisms. Over the past 10 years, this knowledge has translated into a range of targets for therapy, the most promising of which is amyloid β (Aβ). An imbalance between the production and clearance of Aβ is thought by many to represent the earliest event in the pathogenesis of AD. Aβ is known to be subject to oligomerisation, a process that increases its synaptotoxicity. The oligomers may aggregate further to proto-fibrils and fibrils, eventually forming senile plaques, the neuropathological hallmark of AD. In this article we review the key aspects of Aβ as a biomarker for AD, including its pathogenicity, the diagnostic performance of different Aβ assays in different settings, and the potential usefulness of Aβ as a surrogate marker for treatment efficacy in clinical trials of novel Aβ-targeting drugs.
Keywords: Alzheimer's disease, amyloid precursor protein, β-amyloid, biomarker, cerebrospinal fluid, plasma, positron emission tomography
Current Medicinal Chemistry
Title: Amyloid-Related Biomarkers for Alzheimers Disease
Volume: 15 Issue: 8
Author(s): Niels Andreasen and Henrik Zetterberg
Affiliation:
Keywords: Alzheimer's disease, amyloid precursor protein, β-amyloid, biomarker, cerebrospinal fluid, plasma, positron emission tomography
Abstract: Alzheimers disease (AD) is an age-related disorder that causes brain damage resulting in progressive cognitive impairment and death. Three decades of progress have given us a detailed understanding of the underlying molecular mechanisms. Over the past 10 years, this knowledge has translated into a range of targets for therapy, the most promising of which is amyloid β (Aβ). An imbalance between the production and clearance of Aβ is thought by many to represent the earliest event in the pathogenesis of AD. Aβ is known to be subject to oligomerisation, a process that increases its synaptotoxicity. The oligomers may aggregate further to proto-fibrils and fibrils, eventually forming senile plaques, the neuropathological hallmark of AD. In this article we review the key aspects of Aβ as a biomarker for AD, including its pathogenicity, the diagnostic performance of different Aβ assays in different settings, and the potential usefulness of Aβ as a surrogate marker for treatment efficacy in clinical trials of novel Aβ-targeting drugs.
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Cite this article as:
Andreasen Niels and Zetterberg Henrik, Amyloid-Related Biomarkers for Alzheimers Disease, Current Medicinal Chemistry 2008; 15 (8) . https://dx.doi.org/10.2174/092986708783955572
DOI https://dx.doi.org/10.2174/092986708783955572 |
Print ISSN 0929-8673 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-533X |
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