[11C]PBB3 binding in Aβ(–) or Aβ(+) corticobasal syndrome

Abstract

AbstractCorticobasal syndrome (CBS) is associated with 4‐repeat tauopathy and/or Alzheimer's disease pathologies. To examine tau and amyloid‐β (Aβ) deposits in CBS patients using positron emission tomography (PET). Eight CBS patients and three healthy individuals lacking amyloid pathology underwent PET with [11C]PBB3 for tau imaging, and [11C]AZD2184 for Aβ. Subcortical and cortical binding of [11C]PBB3 was compared between Aβ(–) and Aβ(+) CBS patients and reference group. Postmortem analysis was done in one CBS patient. Three CBS patients were considered Aβ(+). Total binding was higher in all patients compared to the reference group. Similar regional binding profiles of [11C]PBB3 in Aβ(+) and Aβ(–) CBS patients were found. Elevated [11C]PBB3 binding in pallidum was observed in all CBS patients. Cortical [11C]PBB3 binding was higher in Aβ(+) compared to Aβ(–) patients. Postmortem analysis of a CBS patient revealed corticobasal degeneration neuropathology and [11C]PBB3 autofluorescence in some tau‐positive structures. [11C]PBB3 is elevated in CBS patients with binding in relevant areas capturing some, but not all, 4‐repeat tauopathy in CBS.