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We read with interest the article by Day et al.,1 which indicated no specific pattern of [18F]-AV-1451 retention was found in patients with rapidly progressive dementia (RPD) resulting from sporadic Creutzfeldt-Jakob disease (sCJD). This finding was in line with a former study that showed that the frequency of tau pathologies could not precisely reflect the deposition of prion protein.2 This work further confirmed that abnormal prion protein deposition in sCJD was not a risk factor for Alzheimer disease (AD), which indicated the [18F]-AV-1451 PET tracer showed a good specificity for paired helical tau filaments observed in AD dementia. In spite of the negative findings of this study, this work may have potential implications concerning the specificity of [18F]-AV-1451 PET retention for paired helical tau filaments. However, a recent study using fluorodeoxyglucose PET (FDG-PET) indicated a close relationship between FDG-PET hypometabolism and neuropathology in cortical, not subcortical, regions in prion disease.3 Further studies are needed to recruit patients with additional causes of RPD to evaluate the clinical applications of in vivo [18F]-AV-1451 PET and FDG-PET imaging in clinical practice.
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Author disclosures are available upon request (journal{at}neurology.org).
- © 2019 American Academy of Neurology
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