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Amyloid imaging in Alzheimer’s disease: a potential new era of personalized medicine?

Antoine Leuzy
  • Translational Neuroimaging Laboratory (TNL), McGill Centre for Studies in Aging (MCSA), Douglas Mental Health University Institute, Montreal, H4H 1R3, Quebec, Canada
  • Alzheimer’s Disease Research Unit, MCSA, Douglas Mental Health University Institute, Montreal, H4H 1R3, Quebec, Canada
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/ Eduardo Zimmer
  • Translational Neuroimaging Laboratory (TNL), McGill Centre for Studies in Aging (MCSA), Douglas Mental Health University Institute, Montreal, H4H 1R3, Quebec, Canada
  • Alzheimer’s Disease Research Unit, MCSA, Douglas Mental Health University Institute, Montreal, H4H 1R3, Quebec, Canada
  • Department of Biochemistry, Federal University of Rio Grande do Sul (UFRGS), Porto Alegre, Brazil
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/ Serge Gauthier
  • Translational Neuroimaging Laboratory (TNL), McGill Centre for Studies in Aging (MCSA), Douglas Mental Health University Institute, Montreal, H4H 1R3, Quebec, Canada
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/ Pedro Rosa-Neto
  • Translational Neuroimaging Laboratory (TNL), McGill Centre for Studies in Aging (MCSA), Douglas Mental Health University Institute, Montreal, H4H 1R3, Quebec, Canada
  • Alzheimer’s Disease Research Unit, MCSA, Douglas Mental Health University Institute, Montreal, H4H 1R3, Quebec, Canada
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Published Online: 2014-03-28 | DOI: https://doi.org/10.2478/s13380-014-0205-y


Recent advances along clinical and neuropathological lines, as well as in our ability to detect the deposition of β-amyloid (Aβ) in vivo using positron emission tomography (PET), have helped redefine Alzheimer’s disease (AD) as a dynamic clinicobiological entity. On the basis of these advances, AD is now conceptualized as a continuum comprising asymptomatic, minimally symptomatic, and dementia phases, with detection of brain Aβ — in particular, via PET amyloid imaging — central to the diagnostic process. In this respect, [18F]florbetapir (Amyvid™) and [18F]flutemetamol (Vizamyl™) have recently received approval for clinical use from the Food and Drug Administration (FDA) and the European Medicines Agency (EMA), with additional radiofluorinated tracers for detection of Aβ in phase III trials. Recent initiatives such as the Alzheimer’s Disease Neuroimaging Initiative (ADNI) suggest that Aβ production, oligomerization and aggregation begins many years, possibly decades, before detectable cognitive impairment, with Aβ shown to associate with cognitive decline and conversion to dementia. While personalized medicine has now emerged as a prospect for the field, the recent decision by the Centers for Medicare & Medicaid Services (CMS) — who declined to cover the cost of amyloid PET imaging citing insufficient evidence to support its clinical utility — highlights that such a move may be premature.

Keywords: Alzheimer’s disease; [11C]PIB [18F]florbetapen; [18F]florbetapir; [18F]flutemetamol; [18F]NAV4694; Amyloid cascade hypothesis; Personalized medicine

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About the article

Published Online: 2014-03-28

Published in Print: 2014-03-01

Citation Information: Translational Neuroscience, Volume 5, Issue 1, Pages 51–56, ISSN (Online) 2081-6936, DOI: https://doi.org/10.2478/s13380-014-0205-y.

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