The positron emission tomography tracer C-deuterium-L-deprenyl (11C-DED) can help physicians visualize astrocytes, which is thought to conspire with amyloid-beta plaques in the progression of Alzheimer disease.
That’s the conclusion of a small Swedish study published in the January edition of the Journal of Nuclear Medicine. It follows closely on the heels of a December 2010 European Journal of Nuclear Medicine and Molecular Imaging study that arrived at similar findings.
In the Swedish study, researchers did a multitracer PET investigation for patients with mild cognitive impairment (MCI), patients with mild Alzheimer disease, and healthy controls using 11C-DED to measure monoamine oxidase B located in astrocytes. Along with 11C-DED PET, data on 11C-Pittsburgh compound B (11C-PIB; fibrillar Aβ deposition), 18F-FDG (18F-fluoro-deoxy-glucose to measure glucose metabolism), MRI, cerebrospinal fluid, and neuropsychologic were acquired from the patients.
11C-DED PET was performed for eight MCI patients, seven Alzheimer disease patients, and 14 healthy controls. 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.
Analysis of the regional 11C-DED binding data revealed increased binding in the bilateral frontal and bilateral parietal cortices of the MCI patients. 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 patients with Alzheimer disease. No regional correlations were found between the three PET tracers.
“Increased 11C-DED binding throughout the brain of the MCI 11C-PIB+ patients potentially suggests that astrocytosis is an early phenomenon in [Alzheimer disease] development,” the researchers wrote.