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Research ArticleClinical Investigations

Evidence for Astrocytosis in Prodromal Alzheimer Disease Provided by 11C-Deuterium-L-Deprenyl: A Multitracer PET Paradigm Combining 11C-Pittsburgh Compound B and 18F-FDG

Stephen F. Carter, Michael Schöll, Ove Almkvist, Anders Wall, Henry Engler, Bengt Långström and Agneta Nordberg
Journal of Nuclear Medicine January 2012, 53 (1) 37-46; DOI: https://doi.org/10.2967/jnumed.110.087031
Stephen F. Carter
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Michael Schöll
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Ove Almkvist
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Anders Wall
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Henry Engler
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Bengt Långström
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Agneta Nordberg
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Abstract

Astrocytes colocalize with fibrillar amyloid-β (Aβ) plaques in postmortem Alzheimer disease (AD) brain tissue. It is therefore of great interest to develop a PET tracer for visualizing astrocytes in vivo, enabling the study of the regional distribution of both astrocytes and fibrillar Aβ. A multitracer PET investigation was conducted for patients with mild cognitive impairment (MCI), patients with mild AD, and healthy controls using 11C-deuterium-L-deprenyl (11C-DED) to measure monoamine oxidase B located in astrocytes. Along with 11C-DED PET, 11C-Pittsburgh compound B (11C-PIB; fibrillar Aβ deposition), 18F-FDG (glucose metabolism), T1 MRI, cerebrospinal fluid, and neuropsychologic data were acquired from the patients. Methods: 11C-DED PET was performed in MCI patients (n = 8; mean age ± SD, 62.6 ± 7.5 y; mean Mini Mental State Examination, 27.5 ± 2.1), AD patients (n = 7; mean age, 65.1 ± 6.3 y; mean Mini Mental State Examination, 24.4 ± 5.7), and healthy age-matched controls (n = 14; mean age, 64.7 ± 3.6 y). A modified reference Patlak model, with cerebellar gray matter as a reference, was chosen for kinetic analysis of the 11C-DED data. 11C-DED data from 20 to 60 min were analyzed using a digital brain atlas. Mean regional 18F-FDG uptake and 11C-PIB retention were calculated for each patient, with cerebellar gray matter as a reference. Results: ANOVA analysis of the regional 11C-DED binding data revealed a significant group effect in the bilateral frontal and bilateral parietal cortices related to increased binding in the MCI patients. All patients, except 3 with MCI, showed high 11C-PIB retention. Increased 11C-DED binding in most cortical and subcortical regions was observed in MCI 11C-PIB+ patients relative to controls, MCI 11C-PIB (negative) patients, and AD patients. No regional correlations were found between the 3 PET tracers. Conclusion: Increased 11C-DED binding throughout the brain of the MCI 11C-PIB+ patients potentially suggests that astrocytosis is an early phenomenon in AD development.

  • Alzheimer disease
  • mild cognitive impairment
  • PET, astrocytosis, amyloid
  • monoamine oxidase B

Footnotes

  • ↵* Contributed equally to this work.

  • © 2012 by the Society of Nuclear Medicine, Inc.
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Journal of Nuclear Medicine: 53 (1)
Journal of Nuclear Medicine
Vol. 53, Issue 1
January 1, 2012
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Evidence for Astrocytosis in Prodromal Alzheimer Disease Provided by 11C-Deuterium-L-Deprenyl: A Multitracer PET Paradigm Combining 11C-Pittsburgh Compound B and 18F-FDG
Stephen F. Carter, Michael Schöll, Ove Almkvist, Anders Wall, Henry Engler, Bengt Långström, Agneta Nordberg
Journal of Nuclear Medicine Jan 2012, 53 (1) 37-46; DOI: 10.2967/jnumed.110.087031

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Evidence for Astrocytosis in Prodromal Alzheimer Disease Provided by 11C-Deuterium-L-Deprenyl: A Multitracer PET Paradigm Combining 11C-Pittsburgh Compound B and 18F-FDG
Stephen F. Carter, Michael Schöll, Ove Almkvist, Anders Wall, Henry Engler, Bengt Långström, Agneta Nordberg
Journal of Nuclear Medicine Jan 2012, 53 (1) 37-46; DOI: 10.2967/jnumed.110.087031
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