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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.

Journal article
Authors Stephen F Carter
Michael Schöll
Ove Almkvist
Anders Wall
Henry Engler
Bengt Långström
Agneta Nordberg
Published in Journal of nuclear medicine : official publication, Society of Nuclear Medicine
Volume 53
Issue 1
Pages 37-46
ISSN 1535-5667
Publication year 2012
Published at
Pages 37-46
Language en
Keywords Aged, Alzheimer Disease, diagnostic imaging, metabolism, pathology, physiopathology, Amyloid beta-Peptides, metabolism, Benzothiazoles, Brain, diagnostic imaging, metabolism, pathology, physiopathology, Case-Control Studies, Cognitive Dysfunction, diagnostic imaging, metabolism, pathology, physiopathology, Deuterium, Female, Fluorodeoxyglucose F18, Gliosis, diagnostic imaging, Humans, Male, Middle Aged, Monoamine Oxidase, metabolism, Neuropsychological Tests, Positron-Emission Tomography, methods, Radioactive Tracers, Retrospective Studies, Selegiline
Subject categories Medical Biotechnology, Clinical Medicine


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 (11)C-deuterium-L-deprenyl ((11)C-DED) to measure monoamine oxidase B located in astrocytes. Along with (11)C-DED PET, (11)C-Pittsburgh compound B ((11)C-PIB; fibrillar Aβ deposition), (18)F-FDG (glucose metabolism), T1 MRI, cerebrospinal fluid, and neuropsychologic data were acquired from the patients.(11)C-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 (11)C-DED data. (11)C-DED data from 20 to 60 min were analyzed using a digital brain atlas. Mean regional (18)F-FDG uptake and (11)C-PIB retention were calculated for each patient, with cerebellar gray matter as a reference.ANOVA analysis of the regional (11)C-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 (11)C-PIB retention. Increased (11)C-DED binding in most cortical and subcortical regions was observed in MCI (11)C-PIB+ patients relative to controls, MCI (11)C-PIB (negative) patients, and AD patients. No regional correlations were found between the 3 PET tracers.Increased (11)C-DED binding throughout the brain of the MCI (11)C-PIB+ patients potentially suggests that astrocytosis is an early phenomenon in AD development.

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