Original Article

European Journal of Nuclear Medicine and Molecular Imaging

, Volume 38, Issue 12, pp 2202-2208

First online:

In vivo imaging of astrocytosis in Alzheimer’s disease: an 11C-L-deuteriodeprenyl and PIB PET study

  • Alexander Frizell SantilloAffiliated withGeriatric Psychiatry, Department of Clinical Medicine, Lund UniversityDepartment of Public Health and Caring Sciences/Geriatrics, Uppsala University Email author 
  • , Juan Pablo GambiniAffiliated withFaculty of Medicine and Faculty of Science, University of the RepublicUruguayan Centre of Molecular Imaging (CUDIM)
  • , Lars LannfeltAffiliated withDepartment of Public Health and Caring Sciences/Geriatrics, Uppsala University
  • , Bengt LångströmAffiliated withDepartments of Biochemistry and Organic Chemistry, Uppsala University
  • , Luohija Ulla-MarjaAffiliated withHelsinki University HospitalDepartment of Medical Sciences, Clinical Physiology, Uppsala University
  • , Lena KilanderAffiliated withDepartment of Public Health and Caring Sciences/Geriatrics, Uppsala University
  • , Henry EnglerAffiliated withFaculty of Medicine and Faculty of Science, University of the RepublicUruguayan Centre of Molecular Imaging (CUDIM)

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Abstract

Purpose

Astrocytosis is an important feature of the neuropathology of Alzheimer’s disease (AD), yet there is currently no way of detecting this phenomenon in vivo.

Methods

In this study we examine the retention of the positron emission tomography (PET) tracer 11C-L-deuteriodeprenyl (DED), thought to bind activated astrocytes, in 9 patients with moderate to severe AD compared with 11 healthy controls. As a measure of amyloid load, 11C-labelled Pittsburgh Compound B (PIB) retention was determined.

Results

Results show a significantly higher 11C-L-DED retention in the frontal (35.1% increase, p = 0.001), parietal (35.2%, p = 0.001), temporal (30.9%, p = 0.0001) and medial temporal lobes (22.3%, p = 0.001) in AD compared to healthy controls after blood flow correction. DED retention in the sensorimotor and occipital cortices, and in white matter and subcortical structures, did not differ between groups. There was a moderate but statistically significant (r = 0.492, p = 0.01) correlation between DED and PIB retention values.

Conclusion

Our conclusion is that DED may serve as an in vivo marker for astrocytosis in AD, providing a window into intermediate processes between amyloidosis and neuronal loss and a means of monitoring immunotherapy.

Keywords

11C-L-deuteriodeprenyl Pittsburgh Compound B Astrocytosis Alzheimer’s disease Positron emission tomography