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2000
Volume 15, Issue 8
  • ISSN: 0929-8673
  • E-ISSN: 1875-533X

Abstract

Alzheimer's 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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/content/journals/cmc/10.2174/092986708783955572
2008-04-01
2025-05-06
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/content/journals/cmc/10.2174/092986708783955572
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