. Investigating astrocytosis with 11C-deuterium Deprenyl in mild cognitive impairment and mild Alzheimer's .A multi-tracer PET paradigm. Human Amyloid Imaging 2011 Meeting Abstracts. 2011 Jan 15;

Abstract:

Background: High amounts of astrocytes co-localise with fibrillar As-plaques in post-mortem AD brains. It is therefore of great interest to develop a PET tracer for visualising reactive astrocytes in Alzheimer's diseasefs earliest stages and study the regional distribution in brain in comparison to fibrillar As. Monoamine oxidase-B (MAO-B) is found primarily in astrocytes. 11C-L-deterium-deprenyl (DED) is a PET tracer with high affinity and specificity for MAO-B. In the current investigation we performed DED-, PIB- and FDG-PET in a group of MCI and AD patients to evaluate the inter-relationship between the three tracers.

Methods: DED-PET was performed in MCI (n = 8; age = 62.6} 7.5; MMSE = 27.5} 2.1) and AD patients (n = 7; age = 65.1} 6.3; MMSE = 24.4} 5.7) and in healthy age matched controls (n = 14; age = 64.7} 3.6), A modified reference-Patlak model, with cerebellar grey matter as reference, was chosen for kinetic analysis of the DED data. Individual DED data from 20-60 minutes was analysed using a digital brain atlas. Mean regional glucose metabolism and PIB uptake ratios were calculated for each patient with cerebellum grey matter as reference.

Results: ANOVA on the regional DED binding data revealed a significant group effect in the bilateral frontal and bilateral parietal cortices. Increased DED binding in most cortical and sub-cortical regions was observed in the MCI patients relative to the controls and AD patients. All patients, except three MCI, were PIB+. Limited regional correlations were found between the three PET tracers particularly between DED and PIB.

Conclusions: Increased DED binding throughout the brain of the MCI patients might suggest that astrocytosis is an early phenomenon in AD development. DED-PET did not correlate with FDG or PIB in most brain regions. To better understand the lack of a strong relationship between the tracers, particularly DED and PIB, requires further investigation with parallel neuroimaging and postmortem studies.

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