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Cerebellar cortical Aβ deposition raises WC reference signals and interferes with CL-based 18F-Florbetapir Aβ PET quantification, which systematically underestimates true cerebral Aβ burden.
Multimodal PET imaging reveals dynamic interactions between cerebral glucose metabolism and dopaminergic degeneration in Parkinson’s disease, highlighting cerebellar-pontine hypermetabolism as a compensatory response to nigrostriatal degeneration.
The pallido-nigro-luysian axis and nigrostriatal system serve as sensitive targets for detecting tau deposition and monoaminergic disruption in PSP and local striatal tau pathology and tau burden were associated with monoaminergic disruption in PSP.
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