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Journal articles on the topic '11C-THK5351'

Author: Grafiati

Published: 3 June 2025

Last updated: 31 July 2025

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1

Miyake, Keisuke, Daisuke Ogawa, and Tetsuhiro Hatakeyama. "STMO-5 Utilization of intraoperative multimodal technologies [PET and 5-ALA] for treating glioblastoma." Neuro-Oncology Advances 3, Supplement_6 (2021): vi12. http://dx.doi.org/10.1093/noajnl/vdab159.044.

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Abstract Background: We can improve prognosis of glioblastoma by using positron emission tomography (PET) scans to guide them in removing tumors, and intraoperative magnetic resonance imaging (IoMRI) and 5-aminolevulinic acid (5-ALA) for identifying residual tumors. Tau proteins are reported to accumulate in glioblastomas, so we compared the efficacy of their PET tracer, THK5351, against that of 11C-MET, 18F-FLT, and 18F-FMISO. Methods: Patients (n = 11) underwent scans between February 2020 and July 2021 for glioblastoma resection. Tumor-to-normal tissue accumulation ratio (TNR) and accumulat

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2

Hatano, Keiko, Kenji Ishibashi, Kazuki Yamada, Kenji Ishii, and Atsushi Iwata. "Clinical Application of 18F-THK5351 PET to Identify Inflammatory Lesions Through Imaging Astrogliosis in a Case of Cytomegalovirus Ventriculoencephalitis." Clinical Nuclear Medicine 48, no. 10 (2023): e489-e490. http://dx.doi.org/10.1097/rlu.0000000000004809.

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Abstract 18F-THK5351 PET is used to estimate the degree of astrogliosis. Because inflammatory lesions usually accompany astrogliosis, 18F-THK5351 PET is potentially worthy of clinical application in inflammatory disorders. Here, we report a case of cytomegalovirus ventriculoencephalitis in an immunocompromised 75-year-old woman who underwent 18F-THK5351 PET and conventional neuroimaging modalities, including 11C-methionine, 18F-FDG, and MRI. 18F-THK5351 PET was clearly superior to the other modalities in identifying inflammatory lesions and can therefore be a useful marker for identifying infl

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3

Nihashi, Takashi, Keita Sakurai, Takashi Kato, et al. "Patterns of Distribution of 18F-THK5351 Positron Emission Tomography in Alzheimer’s Disease Continuum." Journal of Alzheimer's Disease 85, no. 1 (2022): 223–34. http://dx.doi.org/10.3233/jad-215024.

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Background: Alzheimer’s disease (AD) is conceptualized as a biological continuum encompassing the preclinical (clinically asymptomatic but with evidence of AD pathology) and clinical (symptomatic) phases. Objective: Using 18F-THK5351 as a tracer that binds to both tau and monoamine oxidase B (MAO-B), we investigated the changes in 18F-THK5351 accumulation patterns in AD continuum individuals with positive amyloid PET consisting of cognitively normal individuals (CNp), amnestic mild cognitive impairment (aMCI), and AD and cognitively normal individuals (CNn) with negative amyloid PET. Methods:

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4

Ota, Miho, Noriko Sato, Moto Nakaya, et al. "Relationship between the tau protein and choroid plexus volume in Alzheimer’s disease." NeuroReport 34, no. 11 (2023): 546–50. http://dx.doi.org/10.1097/wnr.0000000000001923.

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Tau protein accumulation in the brain is thought to be one of the causes of Alzheimer’s disease (AD). Recent studies found that the choroid plexus (CP) has a role in β-amyloid and tau protein clearance in the brain. We evaluated the relationships between CP volume and the ß-amyloid and tau protein depositions. Participants were 20 patients with AD and 35 healthy subjects who underwent MRI and PET scanning using the ß-amyloid tracer 11C-PiB and the tau/inflammatory tracer 18F-THK5351. We computed the volume of the CP and estimated the relationships between the CP volume and ß-amyloid and tau pr

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5

Chiotis, Konstantinos, Per Stenkrona, Ove Almkvist, et al. "Dual tracer tau PET imaging reveals different molecular targets for 11C-THK5351 and 11C-PBB3 in the Alzheimer brain." European Journal of Nuclear Medicine and Molecular Imaging 45, no. 9 (2018): 1605–17. http://dx.doi.org/10.1007/s00259-018-4012-5.

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6

Higashihara, Mana, Kenji Ishibashi, Aya M. Tokumaru, Kenji Ishii, and Atsushi Iwata. "Brain PET Imaging of 11C-Methionine, 18F-FDG, and 18F-THK5351 in a Case of Lymphomatoid Granulomatosis." Clinical Nuclear Medicine 47, no. 12 (2022): e749-e751. http://dx.doi.org/10.1097/rlu.0000000000004388.

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7

Lemoine, Laetitia, Per-Göran Gillberg, Marie Svedberg, et al. "Comparative binding properties of the tau PET tracers THK5117, THK5351, PBB3, and T807 in postmortem Alzheimer brains." Alzheimer's Research & Therapy 9, no. 1 (2017): 96. https://doi.org/10.1186/s13195-017-0325-z.

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<strong>Background: </strong>The aim of this study was to compare the binding properties of several tau positron emission tomography tracers—THK5117, THK5351, T807 (also known as AV1451; flortaucipir), and PBB3—head to head in the same human brain tissue.<strong>Methods: </strong>Binding assays were performed to compare the regional distribution of <sup>3</sup>H-THK5117 and <sup>3</sup>H-THK5351 in postmortem tissue from three Alzheimer's disease (AD) cases and three control subjects in frontal and temporal cortices as well as in the hippocampus. Competition binding assays between THK5351, THK

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8

Shidahara, Miho, Benjamin A. Thomas, Nobuyuki Okamura, et al. "A comparison of five partial volume correction methods for Tau and Amyloid PET imaging with [18F]THK5351 and [11C]PIB." Annals of Nuclear Medicine 31, no. 7 (2017): 563–69. http://dx.doi.org/10.1007/s12149-017-1185-0.

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9

Ishibashi, Kenji, Masashi Kameyama, Yoshiharu Miura, Jun Toyohara, and Kenji Ishii. "Head-to-Head Comparison of the Two MAO-B Radioligands, 18F-THK5351 and 11C-L-Deprenyl, to Visualize Astrogliosis in Patients With Neurological Disorders." Clinical Nuclear Medicine 46, no. 1 (2020): e31-e33. http://dx.doi.org/10.1097/rlu.0000000000003197.

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10

Mitamura, Katsuya, Takashi Norikane, Yuka Yamamoto, Keisuke Miyake, and Yoshihiro Nishiyama. "Increased Uptake of 18F-THK5351 in Glioblastoma But Not in Metastatic Brain Tumor." Clinical Nuclear Medicine, April 18, 2025. https://doi.org/10.1097/rlu.0000000000005909.

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18F-THK5351 was developed as a tracer with high binding affinity and selectivity for tau protein. However, its off-target binding to monoamine oxidase B (MAO-B), an enzyme highly expressed in astrocytes, has also been demonstrated. In the case of glioblastoma, a strong accumulation of both 11C-methionine (MET) and 18F-THK5351 was observed in the tumor. Conversely, in the case of metastatic brain tumor, while 11C-MET PET showed strong uptake in the lesion, 18F-THK5351 PET revealed no significant accumulation. Differentiating solitary metastatic brain tumors from glioblastoma on MRI can be chall

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11

Mitamura, Katsuya, Takashi Norikane, Yuka Yamamoto, Keisuke Miyake, and Yoshihiro Nishiyama. "Increased Uptake of 18F-THK5351 in Isocitrate Dehydrogenase-Wildtype Glioblastoma But Not in Meningioma." Clinical Nuclear Medicine, July 3, 2024. http://dx.doi.org/10.1097/rlu.0000000000005381.

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Abstract 18F-THK5351 demonstrates a strong binding affinity and selectivity for tau. However, off-target binding with monoamine oxidase-B enzyme, highly expressed in the outer mitochondrial membranes of astrocytes, is possible. In a case with isocitrate dehydrogenase–wildtype glioblastoma, 11C-MET PET and 18F-THK5351 PET exhibited increased uptake in the tumor. Conversely, in another case with intracranial meningioma, MET PET revealed increased uptake in the tumor, whereas 18F-THK5351 PET showed no abnormal uptake in the tumor. However, it is challenging to distinguish meningiomas from gliobla

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12

Ota, Miho, Noriko Sato, Moto Nakaya та ін. "Relationships Between the Deposition of Amyloid-β and Tau Protein and Glymphatic System Activity in Alzheimer’s Disease: Diffusion Tensor Image Study". Journal of Alzheimer's Disease, 15 вересня 2022, 1–9. http://dx.doi.org/10.3233/jad-220534.

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Background: Amyloid-β (Aβ) and tau protein accumulation in the brain is thought to be one of the causes of Alzheimer’s disease (AD). Recent study found that the glymphatic system was waste drainage system in the brain and promoting the elimination of Aβ and tau protein. Objective: Objective: We evaluated the relationships between the glymphatic system activity and Aβ and tau protein deposition. Methods: Subjects were 21 patients with AD and 36 healthy subjects who underwent diffusion tensor imaging (DTI) scan and the positron emission tomography using with the Aβ tracer: 11C-PiB and the tau/in

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13

Ikeda, Masaki, Koichi Okamoto, Keiji Suzuki та ін. "Recurrent Lobar Hemorrhages and Multiple Cortical Superficial Siderosis in a Patient of Alzheimer's Disease With Homozygous APOE ε2 Allele Presenting Hypobetalipoproteinemia and Pathological Findings of 18F-THK5351 Positron Emission Tomography: A Case Report". Frontiers in Neurology 12 (7 липня 2021). http://dx.doi.org/10.3389/fneur.2021.645625.

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In Alzheimer's disease, the apolipoprotein E gene (APOE) ε2 allele is a protective genetic factor, whereas the APOE ε4 allele is a genetic risk factor. However, both the APOE ε2 and the APOE ε4 alleles are genetic risk factors for lobar intracerebral hemorrhage. The reasons for the high prevalence of lobar intracerebral hemorrhage and the low prevalence of Alzheimer's disease with the APOE ε2 allele remains unknown. Here, we describe the case of a 79-year-old Japanese female with Alzheimer's disease, homozygous for the APOE ε2 allele. This patient presented with recurrent lobar hemorrhages and

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14

Kawai, Nobuhiko, Daisuke Ogawa, Tomono Fuke, et al. "Revealing subependymal giant cell astrocytoma with multimodal positron emission tomography: illustrative cases." Journal of Neurosurgery: Case Lessons 8, no. 4 (2024). http://dx.doi.org/10.3171/case24111.

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BACKGROUND There is limited literature on the use of positron emission tomography (PET) for benign tumors originating in the brain ventricles, and the use of multiple tracers for subependymal giant cell astrocytoma (SEGA) has not been reported. The authors compared the PET findings in two SEGA cases with past reports and literature, exploring the distinctive characteristics of SEGA on PET. OBSERVATIONS In a 21-year-old female with SEGA, the authors utilized 18F-fluorodeoxyglucose (18F-FDG), 11C-methionine (11C-MET), 18F-fluorothymidine (18F-FLT), 18F-fluoromisonidazole, and 18F-THK5351 tracers

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15

Ishibashi, Kenji, Masanori Kurihara, Jun Toyohara, Kenji Ishii, and Atsushi Iwata. "Pitfalls of Amyloid-Beta PET." Clinical Nuclear Medicine, February 7, 2024. http://dx.doi.org/10.1097/rlu.0000000000005097.

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Abstract We present 3 patients as pitfalls of amyloid-beta (Aβ) PET, who underwent 11C-PiB (Aβ), 18F-MK-6240 (Alzheimer disease [AD]-tau), and 18F-THK5351 (astrogliosis) PET examinations. Despite negligible or tiny Aβ pathology, patients 1 and 2 were diagnosed with AD as the cause of symptoms. Despite widespread Aβ pathology, patient 3 was not diagnosed with AD as the cause of symptoms. However, if we had only conducted Aβ PET, patients 1 and 2 might not have been diagnosed with AD, whereas patient 3 might have been diagnosed with AD. Hence, both Aβ and AD-tau assessments are necessary to rela

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16

Takaya, Masahiko, Kazunari Ishii, Kazumasa Saigoh, and Osamu Shirakawa. "Longitudinal study of primary progressive aphasia in a patient with pathologically diagnosed Alzheimer’s disease: a case report." Journal of Medical Case Reports 15, no. 1 (2021). http://dx.doi.org/10.1186/s13256-021-02867-6.

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Abstract Background Alzheimer’s disease is a neurodegenerative disease involving the deposition of pathologic amyloid-β and tau protein in the cerebral cortex. Alzheimer’s disease is commonly characterized by progressive impairment of recent memory. Primary progressive aphasia is also often observed in patients with Alzheimer’s disease. Moreover, language-associated symptoms, such as primary progressive aphasia, are diverse and varied in Alzheimer’s disease. However, nonfluent/agrammatic variant primary progressive aphasia is not generally considered a symptom of Alzheimer’s disease. To date,

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17

Li, Yi, Henry Rusinek, Tracy Butler, et al. "Decreased CSF clearance and increased brain amyloid in Alzheimer’s disease." Fluids and Barriers of the CNS 19, no. 1 (2022). http://dx.doi.org/10.1186/s12987-022-00318-y.

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Abstract Background In sporadic Alzheimer’s disease (AD), brain amyloid-beta (Aβ) deposition is believed to be a consequence of impaired Aβ clearance, but this relationship is not well established in living humans. CSF clearance, a major feature of brain glymphatic clearance (BGC), has been shown to be abnormal in AD murine models. MRI phase contrast and intrathecally delivered contrast studies have reported reduced CSF flow in AD. Using PET and tau tracer 18F-THK5117, we previously reported that the ventricular CSF clearance of the PET tracer was reduced in AD and associated with elevated bra

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18

Ozsahin, Ilker, Efe Precious Onakpojeruo, Berna Uzun, Dilber Uzun Ozsahin, and Tracy A. Butler. "Radiopharmaceutical selection for tau PET imaging." Alzheimer's & Dementia 19, S12 (2023). http://dx.doi.org/10.1002/alz.075631.

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AbstractBackgroundThe accumulation of pathologically misfolded tau is a feature that is shared by a group of neurodegenerative disorders that are collectively referred to as tauopathies. AD is the most prevalent of these tauopathies. Neurofibrillary tangles are characterized by the presence of hyperphosphorylated protein (tau), and senile plaques are characterized by the presence of amyloid peptide aggregates. PET imaging is fully quantitative and enables accurate spatial assessment. However, as a result of non‐specific binding and the limited spatial resolution of PET scanners, this technique

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