These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


PUBMED FOR HANDHELDS

Search MEDLINE/PubMed


  • Title: [11 C]PBB3 binding in Aβ(-) or Aβ(+) corticobasal syndrome.
    Author: Cselényi Z, Wallin J, Tjerkoski J, Bloth B, Svensson S, Nennesmo I, Sunnemark D, Jelic V, Farde L, Svenningsson P.
    Journal: Synapse; 2023 Jul; 77(4):e22269. PubMed ID: 36951466.
    Abstract:
    Corticobasal 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 [11 C]PBB3 for tau imaging, and [11 C]AZD2184 for Aβ. Subcortical and cortical binding of [11 C]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 [11 C]PBB3 in Aβ(+) and Aβ(-) CBS patients were found. Elevated [11 C]PBB3 binding in pallidum was observed in all CBS patients. Cortical [11 C]PBB3 binding was higher in Aβ(+) compared to Aβ(-) patients. Postmortem analysis of a CBS patient revealed corticobasal degeneration neuropathology and [11 C]PBB3 autofluorescence in some tau-positive structures. [11 C]PBB3 is elevated in CBS patients with binding in relevant areas capturing some, but not all, 4-repeat tauopathy in CBS.
    [Abstract] [Full Text] [Related] [New Search]