PT - JOURNAL ARTICLE AU - Carter, Stephen F. AU - Schöll, Michael AU - Almkvist, Ove AU - Wall, Anders AU - Engler, Henry AU - Långström, Bengt AU - Nordberg, Agneta TI - Evidence for Astrocytosis in Prodromal Alzheimer Disease Provided by <sup>11</sup>C-Deuterium-<span class="sc">L</span>-Deprenyl: A Multitracer PET Paradigm Combining <sup>11</sup>C-Pittsburgh Compound B and <sup>18</sup>F-FDG AID - 10.2967/jnumed.110.087031 DP - 2012 Jan 01 TA - Journal of Nuclear Medicine PG - 37--46 VI - 53 IP - 1 4099 - http://jnm.snmjournals.org/content/53/1/37.short 4100 - http://jnm.snmjournals.org/content/53/1/37.full SO - J Nucl Med2012 Jan 01; 53 AB - 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.