European Journal of Nuclear Medicine and Molecular Imaging

, Volume 39, Issue 6, pp 990–1000

Longitudinal imaging of Alzheimer pathology using [11C]PIB, [18F]FDDNP and [18F]FDG PET

Authors

    • Department of Neurology & Alzheimer CenterVU University Medical Center
    • Department of Nuclear Medicine & PET ResearchVU University Medical Center
  • Nelleke Tolboom
    • Department of Neurology & Alzheimer CenterVU University Medical Center
    • Department of Nuclear Medicine & PET ResearchVU University Medical Center
  • Jessica C. Foster-Dingley
    • Department of Nuclear Medicine & PET ResearchVU University Medical Center
  • Sofie F. Adriaanse
    • Department of Neurology & Alzheimer CenterVU University Medical Center
    • Department of Nuclear Medicine & PET ResearchVU University Medical Center
  • Ronald Boellaard
    • Department of Nuclear Medicine & PET ResearchVU University Medical Center
  • Maqsood Yaqub
    • Department of Nuclear Medicine & PET ResearchVU University Medical Center
  • Albert D. Windhorst
    • Department of Nuclear Medicine & PET ResearchVU University Medical Center
  • Frederik Barkhof
    • Department of RadiologyVU University Medical Center
  • Adriaan A. Lammertsma
    • Department of Nuclear Medicine & PET ResearchVU University Medical Center
  • Philip Scheltens
    • Department of Neurology & Alzheimer CenterVU University Medical Center
  • Wiesje M. van der Flier
    • Department of Neurology & Alzheimer CenterVU University Medical Center
    • Department of Epidemiology & BiostatisticsVU University Medical Center
  • Bart N. M. van Berckel
    • Department of Nuclear Medicine & PET ResearchVU University Medical Center
Original Article

DOI: 10.1007/s00259-012-2102-3

Cite this article as:
Ossenkoppele, R., Tolboom, N., Foster-Dingley, J.C. et al. Eur J Nucl Med Mol Imaging (2012) 39: 990. doi:10.1007/s00259-012-2102-3

Abstract

Purpose

[11C]PIB and [18F]FDDNP are PET tracers for in vivo detection of the neuropathology underlying Alzheimer’s disease (AD). [18F]FDG is a glucose analogue and its uptake reflects metabolic activity. The purpose of this study was to examine longitudinal changes in these tracers in patients with AD or mild cognitive impairment (MCI) and in healthy controls.

Methods

Longitudinal, paired, dynamic [11C]PIB and [18F]FDDNP (90 min each) and static [18F]FDG (15 min) PET scans were obtained in 11 controls, 12 MCI patients and 8 AD patients. The mean interval between baseline and follow-up was 2.5 years (range 2.0–4.0 years). Parametric [11C]PIB and [18F]FDDNP images of binding potential (BPND) and [18F]FDG standardized uptake value ratio (SUVr) images were generated.

Results

A significant increase in global cortical [11C]PIB BPND was found in MCI patients, but no changes were observed in AD patients or controls. Subsequent regional analysis revealed that this increase in [11C]PIB BPND in MCI patients was most prominent in the lateral temporal lobe (p < 0.05). For [18F]FDDNP, no changes in global BPND were found. [18F]FDG uptake was reduced at follow-up in the AD group only, especially in frontal, parietal and lateral temporal lobes (all p < 0.01). Changes in global [11C]PIB binding (ρ = −0.42, p < 0.05) and posterior cingulate [18F]FDG uptake (ρ = 0.54, p < 0.01) were correlated with changes in Mini-Mental-State Examination score over time across groups, whilst changes in [18F]FDDNP binding (ρ = −0.18, p = 0.35) were not.

Conclusion

[11C]PIB and [18F]FDG track molecular changes in different stages of AD. We found increased amyloid load in MCI patients and progressive metabolic impairment in AD patients. [18F]FDDNP seems to be less useful for examining disease progression.

Keywords

Alzheimer’s diseasePositron emission tomography[11C]PIB[18F]FDDNP[18F]FDG

Copyright information

© Springer-Verlag 2012