THK5351 and flortaucipir PET with pathological correlation in a Creutzfeldt-Jakob disease patient: A case reportopen access
- Authors
- Kim, H.J.[Kim, H.J.]; Cho, H.[Cho, H.]; Park, S.[Park, S.]; Jang, H.[Jang, H.]; Ryu, Y.H.[Ryu, Y.H.]; Choi, J.Y.[Choi, J.Y.]; Moon, S.H.[Moon, S.H.]; Oh, S.J.[Oh, S.J.]; Oh, M.[Oh, M.]; Na, D.L.[Na, D.L.]; Lyoo, C.H.[Lyoo, C.H.]; Kim, E.-J.[Kim, E.-J.]; Seeley, W.W.[Seeley, W.W.]; Kim, J.S.[Kim, J.S.]; Choi, K.C.[Choi, K.C.]; Seo, S.W.[Seo, S.W.]
- Issue Date
- 29-Aug-2019
- Publisher
- BioMed Central Ltd.
- Keywords
- Creutzfeldt-Jakob disease; Flortaucipir PET; Monoamine oxidase B; THK5351 PET
- Citation
- BMC Neurology, v.19, no.1
- Indexed
- SCIE
SCOPUS
- Journal Title
- BMC Neurology
- Volume
- 19
- Number
- 1
- URI
- https://scholarworks.bwise.kr/skku/handle/2021.sw.skku/14586
- DOI
- 10.1186/s12883-019-1434-z
- ISSN
- 1471-2377
- Abstract
- Background: THK5351 and flortaucipir tau ligands have high affinity for paired helical filament tau, yet diverse off-target bindings have been reported. Recent data support the hypothesis that THK5351 binds to monoamine oxidase B (MAO-B) expressed from reactive astrocytes and that flortaucipir has an affinity toward MAO-A and B; however, pathological evidence is lacking. We performed a head-to-head comparison of the two tau ligands in a sporadic Creutzfeldt-Jakob disease (CJD) patient and performed an imaging-pathological correlation study. Case presentation: A 67-year-old man visited our clinic a history of 6 months of rapidly progressive dementia, visual disturbance, and akinetic mutism. Diffusion-weighted imaging showed cortical diffusion restrictions in the left temporo-parieto-occipital regions. 18F-THK5351 PET, but not 18F-flortaucipir PET showed high uptake in the left temporo-parieto-occipital regions, largely overlapping with the diffusion restricted areas. Cerebrospinal fluid analysis was weakly positive for 14-3-3 protein and pathogenic prion protein was found. The patient showed rapid cognitive decline along with myoclonic seizures and died 13 months after his first visit. A post-mortem study revealed immunoreactivity for PrPsc, no evidence of neurofibrillary tangles, and abundant astrocytosis which was reactive for MAO-B antibody. Conclusions: Our findings add pathological evidence that increased THK5351 uptake in sporadic CJD patients might be caused by an off-target binding driven by its high affinity for MAO-B. © 2019 The Author(s).
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