Reduced D2/D3 Receptor Binding and Glucose Metabolism in a Macaque Model of Huntington's Disease

Alison R. Weiss, Daniele Bertoglio, William A. Liguore, Kristin Brandon, John Templon, Jeanne Link, Jodi L. McBride

Research output: Contribution to journalArticlepeer-review


Background: Dopamine system dysfunction and altered glucose metabolism are implicated in Huntington's disease (HD), a neurological disease caused by mutant huntingtin (mHTT) expression. Objective: The aim was to characterize alterations in cerebral dopamine D2/D3 receptor density and glucose utilization in a newly developed AAV-mediated NHP model of HD that expresses mHTT throughout numerous brain regions. Methods: Positron emission tomography (PET) imaging was performed using [18F]fallypride to quantify D2/D3 receptor density and 2-[18F]fluoro-2-deoxy-d-glucose ([18F]FDG) to measure cerebral glucose utilization in these HD macaques. Results: Compared to controls, HD macaques showed significantly reduced dopamine D2/D3 receptor densities in basal ganglia (P < 0.05). In addition, HD macaques displayed significant glucose hypometabolism throughout the cortico-basal ganglia network (P < 0.05). Conclusions: [18F]Fallypride and [18F]FDG are PET imaging biomarkers of mHTT-mediated disease progression that can be used as noninvasive outcome measures in future therapeutic studies with this AAV-mediated HD macaque model.

Original languageEnglish (US)
Pages (from-to)143-147
Number of pages5
JournalMovement Disorders
Issue number1
StatePublished - Jan 2023


  • 2-[F]fluoro-2-deoxy-d-glucose
  • binding potential
  • cortical-basal ganglia
  • fallypride
  • positron emission tomography imaging

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology


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