[18F]-Flortaucipir PET/MRI Supports a 4R Tauopathy Phenotype in Corticobasal Degeneration.
Case report where 18F‑Flortaucipir PET showed asymmetric basal ganglia uptake in an amyloid‑negative patient with corticobasal syndrome, supporting a 4R tauopathy phenotype and suggesting expanded utility of this tracer beyond its current FDA indication.
What the AI sees
Case report where 18F‑Flortaucipir PET showed asymmetric basal ganglia uptake in an amyloid‑negative patient with corticobasal syndrome, supporting a 4R tauopathy phenotype and suggesting expanded utility of this tracer beyond its current FDA indication.
Research significance
Supports use of tau PET as a diagnostic biomarker in 4R tauopathies associated with atypical parkinsonism, which could improve patient selection and outcome measures for tau‑targeted therapeutic development.
Source abstract
A 76-year-old woman presented with progressive left-sided motor incoordination, dystonia, and instability, clinically concerning for atypical parkinsonism. MRI showed Fazekas grade 1 chronic microvascular changes. ¹⁸F-FDG brain PET revealed asymmetric right cerebral hemisphere, sensorimotor cortex, and basal ganglia hypometabolism, suggestive of corticobasal degeneration. ¹⁸F-Florbetapir PET was negative. ¹⁸F-Flortaucipir PET demonstrated asymmetric right basal ganglia uptake, corresponding to hypometabolic regions and contralateral to left-sided symptoms. Although ¹⁸F-Flortaucipir demonstrates limited affinity for pure 4R tau and known off-target subcortical binding, the pronounced asymmetry in this Aβ-negative case of atypical parkinsonism supports a 4R tauopathy phenotype, illustrating potential utility beyond the current FDA-approved indication.