Advertisement
Letter| Volume 441, 120379, October 15, 2022

18F-THK5351 positron emission tomography imaging for Gerstmann-Sträussler-Scheinker disease

  • Yuka Hama
    Affiliations
    Department of Neurology, National Center Hospital, National Center of Neurology and Psychiatry, 4-1-1 Ogawa-higashi, Kodaira, Tokyo 187-8551, Japan
    Search for articles by this author
  • Author Footnotes
    1 Department of Neurology, Tokyo Metropolitan Neurological Hospital, 2–6-1 Musashidai, Fuchu, Tokyo, 183–0042, Japan
    Yuji Saitoh
    Correspondence
    Corresponding author at: Department of Neurology, National Center Hospital, National Center of Neurology and Psychiatry, 4-1-1 Ogawa-higashi, Kodaira, Tokyo 187-8551, Japan.
    Footnotes
    1 Department of Neurology, Tokyo Metropolitan Neurological Hospital, 2–6-1 Musashidai, Fuchu, Tokyo, 183–0042, Japan
    Affiliations
    Department of Neurology, National Center Hospital, National Center of Neurology and Psychiatry, 4-1-1 Ogawa-higashi, Kodaira, Tokyo 187-8551, Japan

    Research Center for Neurocognitive Disorders, National Center Hospital, National Center of Neurology and Psychiatry, 4-1-1 Ogawa-higashi, Kodaira, Tokyo 187-8551, Japan
    Search for articles by this author
  • Etsuko Imabayashi
    Affiliations
    Integrative Brain Imaging Center, National Center of Neurology and Psychiatry, 4-1-1 Ogawa-higashi, Kodaira, Tokyo 187-8551, Japan

    Department of Molecular Imaging and Theranostics, Quantum Life and Medical Science Directorate, National Institute for Quantum Science and Technology, 4-9-1 Anagawa, Inage-ku, Chiba 263-8555, Japan
    Search for articles by this author
  • Yuko Morimoto
    Affiliations
    Department of Neurology, National Center Hospital, National Center of Neurology and Psychiatry, 4-1-1 Ogawa-higashi, Kodaira, Tokyo 187-8551, Japan
    Search for articles by this author
  • Tadashi Tsukamoto
    Affiliations
    Department of Neurology, National Center Hospital, National Center of Neurology and Psychiatry, 4-1-1 Ogawa-higashi, Kodaira, Tokyo 187-8551, Japan

    Research Center for Neurocognitive Disorders, National Center Hospital, National Center of Neurology and Psychiatry, 4-1-1 Ogawa-higashi, Kodaira, Tokyo 187-8551, Japan
    Search for articles by this author
  • Katsuya Sato
    Affiliations
    Department of Locomotive Rehabilitation Science, Nagasaki University Graduate School of Biomedical Sciences, 1-7-1 Sakamoto, Nagasaki 852-8102, Japan
    Search for articles by this author
  • Tetsuyuki Kitamoto
    Affiliations
    Department of Neurological Science, Tohoku University Graduate School of Medicine, 2-1 Seiryo-machi, Aoba-ku, Sendai, Miyagi 980-8575, Japan
    Search for articles by this author
  • Hidehiro Mizusawa
    Affiliations
    Department of Neurology, National Center Hospital, National Center of Neurology and Psychiatry, 4-1-1 Ogawa-higashi, Kodaira, Tokyo 187-8551, Japan
    Search for articles by this author
  • Author Footnotes
    2 Department of Biofunctional Imaging, Fukushima Medical University, 2–2-1 Otemachi, Chiyoda-ku, Tokyo, 100–0004, Japan
    Hiroshi Matsuda
    Footnotes
    2 Department of Biofunctional Imaging, Fukushima Medical University, 2–2-1 Otemachi, Chiyoda-ku, Tokyo, 100–0004, Japan
    Affiliations
    Integrative Brain Imaging Center, National Center of Neurology and Psychiatry, 4-1-1 Ogawa-higashi, Kodaira, Tokyo 187-8551, Japan
    Search for articles by this author
  • Yuji Takahashi
    Affiliations
    Department of Neurology, National Center Hospital, National Center of Neurology and Psychiatry, 4-1-1 Ogawa-higashi, Kodaira, Tokyo 187-8551, Japan
    Search for articles by this author
  • Author Footnotes
    1 Department of Neurology, Tokyo Metropolitan Neurological Hospital, 2–6-1 Musashidai, Fuchu, Tokyo, 183–0042, Japan
    2 Department of Biofunctional Imaging, Fukushima Medical University, 2–2-1 Otemachi, Chiyoda-ku, Tokyo, 100–0004, Japan
Published:August 03, 2022DOI:https://doi.org/10.1016/j.jns.2022.120379
18F-THK5351 positron emission tomography imaging for Gerstmann-Sträussler-Scheinker disease
Previous ArticleA paradox in the video head impulse test
Next ArticleThe possible function and regulation of macrophage migration inhibitory factor (MIF) in multiple sclerosis (MS)
      Gerstmann-Sträussler-Scheinker disease (GSS) is an autosomal dominant prion disease caused by a mutation in the prion protein gene (PRNP). The Pro→Leu mutation at codon 102 of PRNP (P102L) is the most common mutation associated with GSS (GSS-P102L), and patients commonly develop progressive cerebellar ataxia and dementia [
      • Ghetti B.
      • Piccardo P.
      • Zanusso G.
      Dominantly inherited prion protein cerebral amyloidoses - a modern view of Gerstmann-Sträussler-Scheinker.
      Handb. Clin. Neurol. 2018; 153: 243-269
      ]. GSS is pathologically characterized by amyloid plaques consisting of prion protein (PrP) that are primarily observed in the cerebellum and cerebral cortex, astrocytosis, and spongiform degeneration [
      • Ghetti B.
      • Piccardo P.
      • Zanusso G.
      Dominantly inherited prion protein cerebral amyloidoses - a modern view of Gerstmann-Sträussler-Scheinker.
      Handb. Clin. Neurol. 2018; 153: 243-269
      ,
      • Bugiani O.
      • Giaccone G.
      • Piccardo P.
      • Morbin M.
      • Tagliavini F.
      • Ghetti B.
      Neuropathology of Gerstmann-Straussler-Scheinker disease.
      Microsc. Res. Tech. 2000; 50: 10-15
      ]. Although the 18F-THK5351 tracer for positron emission tomography (PET) was originally developed to bind to abnormally deposited tau protein [
      • Harada R.
      • Okamura N.
      • Furumoto S.
      • Furukawa K.
      • Ishiki A.
      • Tomita N.
      • Tago T.
      • Hiraoka K.
      • Watanuki S.
      • Shidahara M.
      • Miyake M.
      • Ishikawa Y.
      • Matsuda R.
      • Inami A.
      • Yoshikawa T.
      • Funaki Y.
      • Iwata R.
      • Tashiro M.
      • Yanai K.
      • Arai H.
      • Kudo Y.
      18F-THK5351: a novel PET radiotracer for imaging neurofibrillary pathology in Alzheimer disease.
      J. Nucl. Med. 2016; 57: 208-214
      ], recent evidence indicates that it exhibits off-target binding to monoamine oxidase-B (MAO-B) expressed in astrocytes [
      • Ng K.P.
      • Pascoal T.A.
      • Mathotaarachchi S.
      • Therriault J.
      • Kang M.S.
      • Shin M.
      • Guiot M.C.
      • Guo Q.
      • Harada R.
      • Comley R.A.
      • Massarweh G.
      • Soucy J.P.
      • Okamura N.
      • Gauthier S.
      • Rosa-Neto P.
      Monoamine oxidase B inhibitor, selegiline, reduces (18)F-THK5351 uptake in the human brain.
      Alzheimers Res. Ther. 2017; 9: 25
      ,
      • Ishiki A.
      • Harada R.
      • Kai H.
      • Sato N.
      • Totsune T.
      • Tomita N.
      • Watanuki S.
      • Hiraoka K.
      • Ishikawa Y.
      • Funaki Y.
      • Iwata R.
      • Furumoto S.
      • Tashiro M.
      • Sasano H.
      • Kitamoto T.
      • Kudo Y.
      • Yanai K.
      • Furukawa K.
      • Okamura N.
      • Arai H.
      Neuroimaging-pathological correlations of [(18)F]THK5351 PET in progressive supranuclear palsy.
      Acta Neuropathol. Commun. 2018; 6: 53
      ]. However, this off-target binding of the 18F-THK5351 tracer to MAO-B-expressing astrocytes can be used to visualize astrogliosis, reflecting neurodegenerative processes other than tauopathy in various neurodegenerative disorders [
      • Kim H.J.
      • Cho H.
      • Park S.
      • Jang H.
      • Ryu Y.H.
      • Choi J.Y.
      • Moon S.H.
      • Oh S.J.
      • Oh M.
      • Na D.L.
      • Lyoo C.H.
      • Kim E.J.
      • Seeley W.W.
      • Kim J.S.
      • Choi K.C.
      • Seo S.W.
      THK5351 and flortaucipir PET with pathological correlation in a Creutzfeldt-Jakob disease patient: a case report.
      BMC Neurol. 2019; 19: 211
      ,
      • Saitoh Y.
      • Imabayashi E.
      • Mukai T.
      • Matsuda H.
      • Takahashi Y.
      Visualization of motor cortex involvement by 18F-THK5351 PET potentially strengthens diagnosis of amyotrophic lateral sclerosis.
      Clin. Nucl. Med. 2021; 46: 243-245
      ]. Here, we report a patient with genetically confirmed GSS harboring the P102L mutation who was examined by 18F-THK5351 PET.

      Keywords

      Abbreviations:

      18F-FDG (18F-2-fluorodeoxy-d-glucose), 99mTc-ECD (99mTc-ethyl cysteinate dimer), DWI (diffusion-weighted imaging), GSS (Gerstmann-Sträussler-Scheinker disease), MAO-B (monoamine oxidase-B), P102L (Pro→Leu mutation at codon 102 of prion protein gene), PET (positron emission tomography), PRNP (prion protein gene), PrP (prion protein), SPECT (single-photon emission computed tomography.), SUV (standardized uptake value), SUVR (standardized uptake value ratio), T1WI (T1-weighted imaging)
      To read this article in full you will need to make a payment

      Purchase one-time access:

      Academic & Personal: 24 hour online accessCorporate R&D Professionals: 24 hour online access
      One-time access price info
      • For academic or personal research use, select 'Academic and Personal'
      • For corporate R&D use, select 'Corporate R&D Professionals'

      Subscribe:

      Subscribe to Journal of the Neurological Sciences
      Already a print subscriber? Claim online access
      Already an online subscriber? Sign in
      Register: Create an account
      Institutional Access: Sign in to ScienceDirect

      References

        • Ghetti B.
        • Piccardo P.
        • Zanusso G.
        Dominantly inherited prion protein cerebral amyloidoses - a modern view of Gerstmann-Sträussler-Scheinker.
        Handb. Clin. Neurol. 2018; 153: 243-269
        View in Article
        • Bugiani O.
        • Giaccone G.
        • Piccardo P.
        • Morbin M.
        • Tagliavini F.
        • Ghetti B.
        Neuropathology of Gerstmann-Straussler-Scheinker disease.
        Microsc. Res. Tech. 2000; 50: 10-15
        View in Article
        • Harada R.
        • Okamura N.
        • Furumoto S.
        • Furukawa K.
        • Ishiki A.
        • Tomita N.
        • Tago T.
        • Hiraoka K.
        • Watanuki S.
        • Shidahara M.
        • Miyake M.
        • Ishikawa Y.
        • Matsuda R.
        • Inami A.
        • Yoshikawa T.
        • Funaki Y.
        • Iwata R.
        • Tashiro M.
        • Yanai K.
        • Arai H.
        • Kudo Y.
        18F-THK5351: a novel PET radiotracer for imaging neurofibrillary pathology in Alzheimer disease.
        J. Nucl. Med. 2016; 57: 208-214
        View in Article
        • Ng K.P.
        • Pascoal T.A.
        • Mathotaarachchi S.
        • Therriault J.
        • Kang M.S.
        • Shin M.
        • Guiot M.C.
        • Guo Q.
        • Harada R.
        • Comley R.A.
        • Massarweh G.
        • Soucy J.P.
        • Okamura N.
        • Gauthier S.
        • Rosa-Neto P.
        Monoamine oxidase B inhibitor, selegiline, reduces (18)F-THK5351 uptake in the human brain.
        Alzheimers Res. Ther. 2017; 9: 25
        View in Article
        • Ishiki A.
        • Harada R.
        • Kai H.
        • Sato N.
        • Totsune T.
        • Tomita N.
        • Watanuki S.
        • Hiraoka K.
        • Ishikawa Y.
        • Funaki Y.
        • Iwata R.
        • Furumoto S.
        • Tashiro M.
        • Sasano H.
        • Kitamoto T.
        • Kudo Y.
        • Yanai K.
        • Furukawa K.
        • Okamura N.
        • Arai H.
        Neuroimaging-pathological correlations of [(18)F]THK5351 PET in progressive supranuclear palsy.
        Acta Neuropathol. Commun. 2018; 6: 53
        View in Article
        • Kim H.J.
        • Cho H.
        • Park S.
        • Jang H.
        • Ryu Y.H.
        • Choi J.Y.
        • Moon S.H.
        • Oh S.J.
        • Oh M.
        • Na D.L.
        • Lyoo C.H.
        • Kim E.J.
        • Seeley W.W.
        • Kim J.S.
        • Choi K.C.
        • Seo S.W.
        THK5351 and flortaucipir PET with pathological correlation in a Creutzfeldt-Jakob disease patient: a case report.
        BMC Neurol. 2019; 19: 211
        View in Article
        • Saitoh Y.
        • Imabayashi E.
        • Mukai T.
        • Matsuda H.
        • Takahashi Y.
        Visualization of motor cortex involvement by 18F-THK5351 PET potentially strengthens diagnosis of amyotrophic lateral sclerosis.
        Clin. Nucl. Med. 2021; 46: 243-245
        View in Article
        • Sugiyama A.
        • Sato N.
        • Kimura Y.
        • Maekawa T.
        • Wakasugi N.
        • Sone D.
        • Enokizono M.
        • Takahashi Y.
        • Murata M.
        • Mizusawa H.
        • Matsuda H.
        Thalamic involvement determined using VSRAD advance on MRI and easy Z-score analysis of (99m)Tc-ECD-SPECT in Gerstmann-Sträussler-Scheinker syndrome with P102L mutation.
        J. Neurol. Sci. 2017; 373: 27-30
        View in Article
        • Arata H.
        • Takashima H.
        • Hirano R.
        • Tomimitsu H.
        • Machigashira K.
        • Izumi K.
        • Kikuno M.
        • Ng A.R.
        • Umehara F.
        • Arisato T.
        • Ohkubo R.
        • Nakabeppu Y.
        • Nakajo M.
        • Osame M.
        • Arimura K.
        Early clinical signs and imaging findings in Gerstmann-Straussler-Scheinker syndrome (Pro102Leu).
        Neurology. 2006; 66: 1672-1678
        View in Article
        • Villemagne V.L.
        • Harada R.
        • Dore V.
        • Furumoto S.
        • Mulligan R.
        • Kudo Y.
        • Burnham S.
        • Krishnadas N.
        • Bozinovski S.
        • Huang K.
        • Lopresti B.J.
        • Yanai K.
        • Rowe C.C.
        • Okamura N.
        First-in-human evaluation of (18)F-SMBT-1, a Novel (18)F-labeled MAO-B PET tracer for imaging reactive astrogliosis.
        J. Nucl. Med. 2022; (Epub ahead of print)https://doi.org/10.2967/jnumed.121.263254
        View in Article

      Article info

      Publication history

      Published online: August 03, 2022
      Accepted: August 1, 2022
      Received in revised form: July 28, 2022
      Received: June 10, 2022

      Identification

      DOI: https://doi.org/10.1016/j.jns.2022.120379

      Copyright

      © 2022 Elsevier B.V. All rights reserved.

      ScienceDirect

      Access this article on ScienceDirect

      The content on this site is intended for healthcare professionals.


      We use cookies to help provide and enhance our service and tailor content. To update your cookie settings, please visit the Cookie Preference Center for this site.
      Copyright © 2023 Elsevier Inc. except certain content provided by third parties.


      RELX