Abstract
The assumption of a rapidly spreading ‘epidemic’ of Alzheimer's disease (AD), the result of aging populations worldwide, coupled with no effective medication for this condition, has incited a move to bring about the prevention of AD before the appearance of clinical symptoms. The following discussion details the establishment of a research conglomerate designed to prevent AD by means of the systematic detection of biomarker changes in healthy middle-aged or younger people. Among the biomarkers currently being standardized are changes in amyloid-β in cerebrospinal fluid (CSF), and deposition of amyloid-β plaques in the living brain detectable by means of brain scans. Possession of one specific allele of the APOE gene is an additional biomarker. However, these molecular features are merely indicators of increased risk, and pre-symptomatic dementia cannot be definitively diagnosed on the basis of the presence of one or more of them. The composition, distribution, and function of the key molecule being tracked, amyloid-β, remains poorly understood and, highly significant, a large number of individuals with a heavy amyloid load in their brains live to old age with no behavioral signs of dementia. The concluding section considers preparations for a randomized controlled trial designed to detect and eliminate amyloid-β deposition very early in its formation.
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Acknowledgements
An earlier version of this article was presented at a conference held at the University of Vienna, July 2012, organized by Herbert Gottweis titled ‘Towards Personalized Medicine? Biomarkers in Practice’.
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A number of proofing corrections were not included in the version of this article originally published 22 April 2013. These corrections have been made in this final version.
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Lock, M. Detecting amyloid biomarkers: Embodied risk and Alzheimer prevention. BioSocieties 8, 107–123 (2013). https://doi.org/10.1057/biosoc.2013.5
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DOI: https://doi.org/10.1057/biosoc.2013.5