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Anne M. Remes, MD, PhD; Lauri Laru, MSc; Hannu Tuominen, MD, PhD; Sargo Aalto, MSc; Nina Kemppainen, MD, PhD; Helinä Mononen, MA; Kjell Någren, PhD; Riitta Parkkola, MD, PhD; Juha O. Rinne, MD, PhD

Arch Neurol. 2008;65(4):540-544.

Objective  To investigate amyloid accumulation by carbon 11–labeled Pittsburgh Compound B (¹¹C-PiB) in hereditary cerebral amyloid angiopathy and APP locus duplication.

Design, Setting, and Patients  Positron emission tomography with ¹¹C-PiB and magnetic resonance imaging were performed for 2 patients, 49-year-old and 60-year-old siblings with APP locus duplication, with hereditary Alzheimer disease and cerebral amyloid angiopathy.

Main Outcome Measure  Change in ¹¹C-PiB uptake.

Results  Uptake of ¹¹C-PiB was increased especially in the striatum (caudate nucleus to 225% and 280% of the control mean and putamen to 166% and 185% of the control mean) and in the posterior cingulate (to 168% and 198% of the control mean), and it was marginally increased in other cortical brain areas. The pattern of increased ¹¹C-PiB uptake was different from that seen in sporadic Alzheimer disease.

Conclusions  Amyloid imaging with ¹¹C-PiB positron emission tomography is a useful tool for detecting in vivo amyloid accumulation in patients with hereditary cerebral amyloid angiopathy. However, the pattern of ¹¹C-PiB accumulation differs between patients with typical AD and patients with APP locus duplication.

Author Affiliations: Clinical Research Centre, Oulu University Hospital (Dr Remes and Mr Laru), and Departments of Neurology (Dr Remes, Mr Laru, and Ms Mononen) and Pathology (Dr Tuominen), University of Oulu, Oulu, Finland; and Department of Psychology, Åbo Akademi University (Mr Aalto), Turku PET Centre, University of Turku (Mr Aalto and Drs Kemppainen, Någren, and Rinne), and Departments of Neurology (Dr Kemppainen) and Radiology (Dr Parkkola), Turku University Hospital, Turku, Finland.

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