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1

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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2

Lemoine, Laetitia, Laure Saint-Aubert, Amelia Marutle, et al. "Visualization of regional tau deposits using 3H-THK5117 in Alzheimer brain tissue." Acta Neuropathologica Communications 3 (July 2, 2015): 40. https://doi.org/10.1186/s40478-015-0220-4.

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INTRODUCTION: The accumulation of neurofibrillary tangles, composed of aggregated hyperphosphorylated tau protein, starts spreading early in specific regions in the course of Alzheimer&#39;s disease (AD), correlating with the progression of memory dysfunction. The non-invasive imaging of tau could therefore facilitate the early diagnosis of AD, differentiate it from other dementing disorders and allow evaluation of tau immunization therapy outcomes. In this study we characterized the in vitro binding properties of THK5117, a tentative radiotracer for positron emission tomography (PET) imaging
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3

Villemange, Victor, Christopher Rowe, Gilles Tamagnan, et al. "IN VIVO TAU IMAGING WITH 18F-THK5105 AND 18F-THK5117." Alzheimer's & Dementia 10 (July 2014): P241. http://dx.doi.org/10.1016/j.jalz.2014.04.363.

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4

Lemoine, Laetitia, Laure Saint-Aubert, Inger Nennesmo, Per-Göran Gillberg, and Agneta Nordberg. "Cortical laminar tau deposits and activated astrocytes in Alzheimer's disease visualised by 3H-THK5117 and 3H-deprenyl autoradiography." Scientific Reports 7 (April 4, 2017): 45496. https://doi.org/10.1038/srep45496.

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Abstract Hyperphosphorylated tau protein deposits and, inflammatory processes are characteristic components of Alzheimer disease (AD) pathology. We here aimed to visualize in vitro the distribution of tau deposits and activated astrocytes across the cortical layers in autopsy AD brain tissue using the radiotracers <sup>3</sup>H-THK5117 and <sup>3</sup>H-deprenyl. <sup>3</sup>H-THK5117 and <sup>3</sup>H-deprenyl autoradiographies were carried out on frozen brain sections from three AD patients and one healthy control. <sup>3</sup>H-THK5117 showed a distinct laminar cortical binding similar to <
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5

Chiotis, Konstantinos, Laure Saint-Aubert, Irina Savitcheva, et al. "Imaging in-vivo tau pathology in Alzheimer's disease with THK5317 PET in a multimodal paradigm." Eur J Nucl Med Mol Imaging 43, no. 9 (2016): 1686–99. https://doi.org/10.1007/s00259-016-3363-z.

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PURPOSE: The aim of this study was to explore the cerebral distribution of the&nbsp;tau-specific PET tracer [(18)F]THK5317 (also known as (S)-[(18)F]THK5117) retention in different stages of Alzheimer&#39;s disease; and study any associations with markers of hypometabolism and amyloid-beta deposition. METHODS: Thirty-three individuals were enrolled, including nine patients with Alzheimer&#39;s disease dementia, thirteen with mild cognitive impairment (MCI), two with non-Alzheimer&#39;s disease dementia, and nine healthy controls (five young and four elderly). In a multi-tracer PET design [(18)
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6

Zimmer, Eduardo Rigon, Antoine Leuzy, Serge Gauthier, and Pedro Rosa-Neto. "Developments in Tau PET Imaging." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 41, no. 5 (2014): 547–53. http://dx.doi.org/10.1017/cjn.2014.15.

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ABSTRACTThe presence of neurofibrillary tangles in the brain is a hallmark feature of several neurodegenerative diseases termed “tauopathies,” including Alzheimer’s disease (AD) and the tau molecular subgroup of frontotemporal lobar degeneration (FTLD-tau). Recently, several positron emission tomography (PET) radiopharmaceuticals targeting abnormal conformations of the tau protein have been developed. To date, six novel tau imaging agents—[18F]THK523, [18F]THK5105, [18F]THK5117, [18F]T807, [18F]T808, and [11C]PBB3—have been described and are considered promising as potential tau radioligands.
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7

Jonasson, My, Anders Wall, Konstantinos Chiotis, et al. "Tracer kinetic analysis of (S)-18F-THK5117 as a PET tracer for assessing tau pathology." Journal of Nuclear Medecine 57, no. 4 (2016): 574–81. https://doi.org/10.2967/jnumed.115.158519.

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Because a correlation between tau pathology and the clinical symptoms of Alzheimer&#39;s disease (AD) has been hypothesized, there is increasing interest in developing PET tracers that bind specifically to tau protein. The aim of this study was to evaluate tracer kinetic models for quantitative analysis and generation of parametric images for the novel tau ligand (S)-<sup>18</sup>F-THK5117. METHODS: 9 subjects (5 with AD, 4 with mild cognitive impairment) received a 90 min dynamic (S)-<sup>18</sup>F-THK5117 PET scan. Arterial blood was sampled for measurement of blood radioactivity and metabol
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8

Jonasson, M., A. Wall, K. Chiotis, et al. "Tracer Kinetic Analysis of (S)-18F-THK5117 as a PET Tracer for Assessing Tau Pathology." Journal of Nuclear Medicine 57, no. 4 (2016): 574–81. http://dx.doi.org/10.2967/jnumed.115.158519.

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9

Brendel, M., A. Jaworska, F. Probst, et al. "Small-Animal PET Imaging of Tau Pathology with 18F-THK5117 in 2 Transgenic Mouse Models." Journal of Nuclear Medicine 57, no. 5 (2016): 792–98. http://dx.doi.org/10.2967/jnumed.115.163493.

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10

Harada, Ryuichi, Nobuyuki Okamura, Shozo Furumoto, et al. "P1-010: BINDING CHARACTERIZATION OF TAU PET TRACER 18F-THK5117 IN NON-ALZHEIMER'S NEURODEGENERATIVE DISEASES." Alzheimer's & Dementia 10 (July 2014): P307—P308. http://dx.doi.org/10.1016/j.jalz.2014.05.245.

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11

Lemoine, Laetitia, Konstantinos Chiotis, Antoine Leuzy, Inger Nennesmo, and Agneta K. Nordberg. "P4-599: ANTE-MORTEM BINDING OF 18 F-THK5317 PET IN A CASE OF FTLD AND POST-MORTEM COMPARISON OF TAU BINDING USING 3 H-THK5117 AND 3 H-MK6240." Alzheimer's & Dementia 15 (July 2019): P1554. http://dx.doi.org/10.1016/j.jalz.2019.08.147.

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12

Lemoine, Laetitia, Per-Göran Gillberg, Marie Svedberg, et al. "COMPARISON OF BINDING PROPERTIES OF THK5117, THK5351, PBB3 AND T807 IN AUTOPSIES OF ALZHEIMER DISEASE CASES." Alzheimer's & Dementia 13, no. 7 (2017): P139—P140. http://dx.doi.org/10.1016/j.jalz.2017.06.2564.

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13

Okamura, Nobuyuki, Ryuichi Harada, Shozo Furumoto, et al. "IC-P-215: COMPARISON OF 18F-THK5117 AND 11C-PIB PET IMAGES IN PATIENTS WITH ALZHEIMER'S DISEASE." Alzheimer's & Dementia 10 (July 2014): P116. http://dx.doi.org/10.1016/j.jalz.2014.05.223.

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14

Lemoine, Laetitia, Per-Göran Gillberg, Marie Svedberg, et al. "[P4-274]: COMPARISON OF BINDING PROPERTIES OF THK5117, THK5351, PBB3 AND T807 IN AUTOPSIES OF ALZHEIMER DISEASE CASES." Alzheimer's & Dementia 13, no. 7S_Part_28 (2017): P1390. http://dx.doi.org/10.1016/j.jalz.2017.06.2143.

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15

Lemoine, Laetitia, Per-Göran Gillberg, Amelia Marutle, et al. "O1-12-04: CHARACTERIZATION OF THK5117 BINDING IN AD BRAIN TISSUE: IMPLICATION FOR DEVELOPMENT OF PET TAU IMAGING." Alzheimer's & Dementia 10 (July 2014): P155. http://dx.doi.org/10.1016/j.jalz.2014.04.125.

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16

Lemoine, Laetitia, Per-Göran Gillberg, Amelia Marutle, et al. "IC-P-212: CHARACTERIZATION OF THK5117 BINDING IN AD BRAIN TISSUE: IMPLICATION FOR DEVELOPMENT OF PET TAU IMAGING." Alzheimer's & Dementia 10 (July 2014): P115. http://dx.doi.org/10.1016/j.jalz.2014.05.220.

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17

Rodriguez-Vieitez, Elena, Antoine Leuzy, Konstantinos Chiotis, Laure Saint-Aubert, and Agneta Nordberg. "Comparison of Early-Phase (S)-[18F]THK5117 and [11C]PIB PET imaging to assess brain perfusion in Alzheimer’s disease." Neurobiology of Aging 39 (March 2016): S21. http://dx.doi.org/10.1016/j.neurobiolaging.2016.01.095.

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18

Alzghool, Obada M., Johanna Rokka, Francisco R. López-Picón та ін. "(S)-[18F]THK5117 brain uptake is associated with Aβ plaques and MAO-B enzyme in a mouse model of Alzheimer's disease". Neuropharmacology 196 (вересень 2021): 108676. http://dx.doi.org/10.1016/j.neuropharm.2021.108676.

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19

Nordberg, Agneta. "O4-07-05: 18F-(S).THK5117 as a PET tracer for tau pathology in Alzheimer's disease and non-alzheimer's disease dementia." Alzheimer's & Dementia 11, no. 7S_Part_6 (2015): P285. http://dx.doi.org/10.1016/j.jalz.2015.07.385.

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20

Johnson, Sterling C., Tobey J. Betthauser, Patrick J. Lao, et al. "O5-01-05: Tau and amyloid imaging in presymptomatic and symptomatic Alzheimer's disease with [F-18]THK5117 and [C-11]PiB: A multimodal imaging study." Alzheimer's & Dementia 11, no. 7S_Part_7 (2015): P314. http://dx.doi.org/10.1016/j.jalz.2015.07.449.

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21

Rodriguez-Vieitez, Elena, Antoine Leuzy, Konstantinos Chiotis, Laure Saint-Aubert, Anders Wall, and Agneta Nordberg. "Comparability of [18F]THK5317 and [11C]PIB blood flow proxy images with [18F]FDG positron emission tomography in Alzheimer’s disease." Journal of Cerebral Blood Flow & Metabolism 37, no. 2 (2016): 740–49. http://dx.doi.org/10.1177/0271678x16645593.

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For amyloid positron emission tomography tracers, the simplified reference tissue model derived ratio of influx rate in target relative to reference region (R1) has been shown to serve as a marker of brain perfusion, and, due to the strong coupling between perfusion and metabolism, as a proxy for glucose metabolism. In the present study, 11 prodromal Alzheimer’s disease and nine Alzheimer’s disease dementia patients underwent [18F]THK5317, carbon-11 Pittsburgh Compound-B ([11C]PIB), and 2-deoxy-2-[18F]fluoro-D-glucose ([18F]FDG) positron emission tomography to assess the possible use of early-
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22

Rodriguez-Vieitez, Elena, Antoine Leuzy, Konstantinos Chiotis, Laure Saint-Aubert, Anders Wall, and Agneta Nordberg. "Comparability of [18F]THK5317 and [11C]PIB blood flow proxy images with [18F]FDG positron emission tomography in Alzheimer's disease." Journal of Cerebral Blood Flow and Metabolism 37, no. 2 (2016): 740–49. https://doi.org/10.1177/0271678X16645593.

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For amyloid positron emission tomography tracers, the simplified reference tissue model derived ratio of influx rate in target relative to reference region (R<sub>1</sub>) has been shown to serve as a marker of brain perfusion, and, due to the strong coupling between perfusion and metabolism, as a proxy for glucose metabolism. In the present study, 11 prodromal Alzheimer&#39;s disease and nine Alzheimer&#39;s disease dementia patients underwent [<sup>18</sup>F]THK5317, carbon-11 Pittsburgh Compound-B ([<sup>11</sup>C]PIB), and 2-deoxy-2-[<sup>18</sup>F]fluoro-D-glucose ([<sup>18</sup>F]FDG) po
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23

Saint-Aubert, Laure, Ove Almkvist, Konstantinos Chiotis, Rita Almeida, Anders Wall, and Agneta Nordberg. "Regional tau deposition measured by [18F]THK5317 positron emission tomography is associated to cognition via glucose metabolism in Alzheimer's disease." Alzheimer's Research & Therapy 8, no. 1 (2016): 38. https://doi.org/10.1186/s13195-016-0204-z.

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BACKGROUND: The recent development of tau-specific positron emission tomography (PET) tracers has allowed in vivo quantification of regional tau deposition and offers the opportunity to monitor the progression of tau pathology along with cognitive impairment. In this study, we investigated the relationships of cerebral tau deposition ([<sup>18</sup>F]THK5317-PET) and metabolism ([<sup>18</sup>F]FDG-PET) with concomitant cognitive function in patients with probable Alzheimer&#39;s disease (AD). METHODS: Nine patients diagnosed with AD dementia and 11 with prodromal AD (mild cognitive impairment
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24

Lemoine, Laetitia, Martin Ingelsson, Inger Nennesmo, Per-Göran Gillberg, and Agneta Nordberg. "In vitro characterization of fibrillar amyloid, tau deposits, and activated astrocytes in Arctic APP and sporadic Alzheimer's disease brain using, 3H-PIB and 3H-THK5117 and 3H-Deprenyl in comparison to immunostaining." Neurobiology of Aging 39 (March 2016): S15. http://dx.doi.org/10.1016/j.neurobiolaging.2016.01.073.

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25

Lemoine, Laetitia, Martin Ingelsson, Inger Nennesmo, Per-Goran Gillberg, and Agneta Nordberg. "IC-P-170: In Vitro Characterization of Fibrillar Amyloid, TAU Deposition, and Activated Astrocytes in Arctic AD Brain in Comparison With Sporadic AD Brain Using 3H-PIB, 3H-THK5117 and 3H-Deprenyl." Alzheimer's & Dementia 12 (July 2016): P124. http://dx.doi.org/10.1016/j.jalz.2016.06.201.

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26

Lemoine, Laetitia, Martin Ingelsson, Inger Nennesmo, Per-Goran Gillberg, and Agneta Nordberg. "P1-105: In vitro Characterization of Fibrillar Amyloid, TAU Deposition, and Activated Astrocytes in Arctic Alzheimer's Disease Brain in Comparison With Sporadic Alzheimer's Disease Brain Using 3H-PIB, 3H-THK5117 and 3H-DEPRENYL." Alzheimer's & Dementia 12 (July 2016): P442. http://dx.doi.org/10.1016/j.jalz.2016.06.853.

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27

Doré, Vincent, Pierrick Bourgeat, Jurgen Fripp, et al. "IC-P-170: Interaction between 18 F-THK5317, 18 F-flutemetamol SUVR and cortical thickness." Alzheimer's & Dementia 11, no. 7S_Part_2 (2015): P113. http://dx.doi.org/10.1016/j.jalz.2015.06.193.

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28

Doré, Vincent, Pierrick Bourgeat, Jurgen Fripp, et al. "O5-01-03: Interaction between 18 F-THK5317, 18 F-flutemetamol SUVR, and cortical thickness." Alzheimer's & Dementia 11, no. 7S_Part_7 (2015): P313. http://dx.doi.org/10.1016/j.jalz.2015.07.447.

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29

Chiotis, Konstantinos, Laure Saint-Aubert, Irina Savitcheva, et al. "Imaging in-vivo tau pathology in Alzheimer’s disease with THK5317 PET in a multimodal paradigm." European Journal of Nuclear Medicine and Molecular Imaging 43, no. 9 (2016): 1686–99. http://dx.doi.org/10.1007/s00259-016-3363-z.

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30

Okamura, Nobuyuki, Shozo Furumoto, Michelle T. Fodero-Tavoletti, et al. "Non-invasive assessment of Alzheimer’s disease neurofibrillary pathology using 18F-THK5105 PET." Brain 137, no. 6 (2014): 1762–71. http://dx.doi.org/10.1093/brain/awu064.

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31

Jonasson, My, Anders Wall, Konstantinos Chiotis, et al. "Optimal timing of tau pathology imaging and automatic extraction of a reference region using dynamic [18F]THK5317 PET." NeuroImage: Clinical 22 (2019): 101681. http://dx.doi.org/10.1016/j.nicl.2019.101681.

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32

Saint-Aubert, Laure, Konstantinos Chiotis, Anders Wall, Ove Almkvist, and Agneta Nordberg. "P1-306: Association Between in Vivo TAU Deposition Measured Using [18F]THK5317 Pet and Cognitive Functions in Alzheimer's Disease." Alzheimer's & Dementia 12 (July 2016): P539—P540. http://dx.doi.org/10.1016/j.jalz.2016.06.1056.

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33

Saint-Aubert, Laure, Laetitia Lemoine, Konstantinos Chiotis, Antoine Leuzy, Elena Rodriguez-Vieitez, and Agneta Nordberg. "Tau PET imaging: present and future directions." Molecular Neurodegeneration 12, no. 1 (2017): 19. https://doi.org/10.1186/s13024-017-0162-3.

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Abnormal aggregation of tau in the brain is a major contributing factor in various neurodegenerative diseases. The role of tau phosphorylation in the pathophysiology of tauopathies remains unclear. Consequently, it is important to be able to accurately and specifically target tau deposits in vivo in the brains of patients. The advances of molecular imaging in the recent years have now led to the recent development of promising tau-specific tracers for positron emission tomography (PET), such as THK5317, THK5351, AV-1451, and PBB3. These tracers are now available for clinical assessment in pati
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34

Lee, Hyunjong, Yuna Gu, Sang Won Seo, and Seung Hwan Moon. "Tau positron emission tomography in tauopathies: A narrative review." Precision and Future Medicine 7, no. 1 (2023): 7–24. http://dx.doi.org/10.23838/pfm.2023.00016.

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Aggregation of misfolded tau in the brain is a major pathological feature common in various neurodegenerative disorders known as tauopathies, including Alzheimer’s disease, progressive supranuclear palsy, corticobasal syndrome, and dementia with Lewy bodies. Tauopathies are collection of diseases with varied overlapping symptoms and complicated manifestations. Consequently, it is crucial to be able to assess tau deposits &lt;i&gt;in vivo&lt;/i&gt;. Over the past decade, tau-specific radioligands for positron emission tomography (PET) have been developed and tested, including first-generation c
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35

Ferreira Schopf, Patricia, Ivana Zanella, M. Natália D. S. Cordeiro, Juan M. Ruso, Michael González-Durruthy, and Mirkos Ortiz Martins. "Nanomarker for Early Detection of Alzheimer’s Disease Combining Ab initio DFT Simulations and Molecular Docking Approach." Biophysica 1, no. 2 (2021): 76–86. http://dx.doi.org/10.3390/biophysica1020007.

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The tau protein is considered an important qualitative and quantitative biomarker for Alzheimer’s disease in its asymptomatic phase. In 2011, biomarkers were suggested by the National Institute on Aging-Azheimer’s Association as a new criterion for the early diagnosis of Alzheimer’s disease. Thus, highlighting the non-existence of theoretical research on the subject, we investigated the binding interaction properties between phosphorylated tau protein and a theoretically modeled ligands constituted by the fullerol functionalized with radiopharmaceuticals from an in silico approach via molecula
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36

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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37

Lemoine, L., A. Ledreux, E. J. Mufson, et al. "Regional binding of tau and amyloid PET tracers in Down syndrome autopsy brain tissue." Molecular Neurodegeneration 15, no. 1 (2020). http://dx.doi.org/10.1186/s13024-020-00414-3.

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Abstract Introduction Tau pathology is a major age-related event in Down syndrome with Alzheimer’s disease (DS-AD). Although recently, several different Tau PET tracers have been developed as biomarkers for AD, these tracers showed different binding properties in Alzheimer disease and other non-AD tauopathies. They have not been yet investigated in tissue obtained postmortem for DS-AD cases. Here, we evaluated the binding characteristics of two Tau PET tracers (3H-MK6240 and 3H-THK5117) and one amyloid (3H-PIB) ligand in the medial frontal gyrus (MFG) and hippocampus (HIPP) in tissue from adul
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38

Lemoine, Laetitia, Laure Saint-Aubert, Amelia Marutle, et al. "Visualization of regional tau deposits using 3H-THK5117 in Alzheimer brain tissue." Acta Neuropathologica Communications 3, no. 1 (2015). http://dx.doi.org/10.1186/s40478-015-0220-4.

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39

Chaney, A.M., F.R. Lopez-Picon, S. Serriere, et al. "Prodromal neuroinflammatory, cholinergic and metabolite dysfunction detected by PET and MRS in the TgF344-AD transgenic rat model of AD: a collaborative multi-modal study." Theranostics Online advance article (February 15, 2021). https://doi.org/10.7150/thno.56059.

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<strong>ABSTRACT</strong> Mouse models of Alzheimer&rsquo;s disease (AD) are valuable but do not fully recapitulate human AD pathology, such as spontaneous Tau fibril accumulation and neuronal loss, necessitating the development of new AD models. The transgenic (TG) TgF344-AD rat has been reported to develop age-dependent AD features including neuronal loss and neurofibrillary tangles, despite only expressing APP and PSEN1 mutations, suggesting an improved modelling of AD hallmarks. Alterations in neuronal networks as well as learning performance and cognition tasks have been reported in this
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40

Brendel, Matthias, Behrooz H. Yousefi, Tanja Blume, et al. "Comparison of 18F-T807 and 18F-THK5117 PET in a Mouse Model of Tau Pathology." Frontiers in Aging Neuroscience 10 (June 7, 2018). http://dx.doi.org/10.3389/fnagi.2018.00174.

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41

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). http://dx.doi.org/10.1186/s13195-017-0325-z.

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42

Lemoine, Laetitia, Laure Saint-Aubert, Inger Nennesmo, Per-Göran Gillberg, and Agneta Nordberg. "Cortical laminar tau deposits and activated astrocytes in Alzheimer’s disease visualised by 3H-THK5117 and 3H-deprenyl autoradiography." Scientific Reports 7, no. 1 (2017). http://dx.doi.org/10.1038/srep45496.

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43

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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44

Leuzy, Antoine, Elena Rodriguez-Vieitez, Laure Saint-Aubert, et al. "Longitudinal uncoupling of cerebral perfusion, glucose metabolism, and tau deposition in Alzheimer's disease." Alzheimer's & Dementia, December 19, 2017. https://doi.org/10.1016/j.jalz.2017.11.008.

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Abstract INTRODUCTION: Cross-sectional findings using the tau tracer [<sup>18</sup>F]THK5317 (THK5317) have shown that [<sup>18</sup>F]fluorodeoxyglucose (FDG) positron emission tomography (PET) data can be approximated using perfusion measures (early-frame standardized uptake value ratio; ratio of tracer delivery in target to reference regions). In this way, a single PET study can provide both functional and molecular information. METHODS: We included 16 patients with Alzheimer&#39;s disease who completed follow-up THK5317 and FDG studies 17 months after baseline investigations. Linear mixed-
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45

Malarte, Mona-Lisa, Agneta Nordberg, and Laetitia Lemoine. "Characterization of MK6240, a tau PET tracer, in autopsy brain tissue from Alzheimer’s disease cases." European Journal of Nuclear Medicine and Molecular Imaging, September 24, 2020. http://dx.doi.org/10.1007/s00259-020-05035-y.

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Abstract Purpose MK6240 is a second-generation tau PET tracer designed to detect the neurofibrillary tangles in the brains of patients with Alzheimer’s disease (AD). The aim of the study was to characterize 3H-MK6240 in AD and control brain tissue and to compare its binding properties with those of first-generation tau PET tracers. Methods Saturation binding assays with 3H-MK6240 were carried out in the temporal and parietal cortices of AD brains to determine the maximum number of binding sites (Bmax) and the dissociation constants (Kd) at these sites. Competitive binding assays were carried o
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Colato, Elisa, Konstantinos Chiotis, Daniel Ferreira, et al. "Assessment of Tau Pathology as Measured by 18F-THK5317 and 18F-Flortaucipir PET and Their Relation to Brain Atrophy and Cognition in Alzheimer’s Disease." Journal of Alzheimer's Disease, September 9, 2021, 1–15. http://dx.doi.org/10.3233/jad-210614.

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Background: In Alzheimer’s disease (AD), the abnormal aggregation of hyperphosphorylated tau leads to synaptic dysfunction and neurodegeneration. Recently developed tau PET imaging tracers are candidate biomarkers for diagnosis and staging of AD. Objective: We aimed to investigate the discriminative ability of 18F-THK5317 and 18F-flortaucipir tracers and brain atrophy at different stages of AD, and their respective associations with cognition. Methods: Two cohorts, each including 29 participants (healthy controls [HC], prodromal AD, and AD dementia patients), underwent 18F-THK5317 or 18F-flort
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Chiotis, K., L. Saint-Aubert, E. Rodriguez-Vieitez, et al. "Longitudinal changes of tau PET imaging in relation to hypometabolism in prodromal and Alzheimer's disease dementia." Molecular Psychiatry, May 16, 2017. https://doi.org/10.1038/mp.2017.108.

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Abstract The development of tau-specific positron emission tomography (PET) tracers allows imaging in vivo the regional load of tau pathology in Alzheimer&#39;s disease (AD) and other tauopathies. Eighteen patients with baseline investigations enroled in a 17-month follow-up study, including 16 with AD (10 had mild cognitive impairment and a positive amyloid PET scan, that is, prodromal AD, and six had AD dementia) and two with corticobasal syndrome. All patients underwent PET scans with [<sup>18</sup>F]THK5317 (tau deposition) and [<sup>18</sup>F]FDG (glucose metabolism) at baseline and follo
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Fu, Liping, Zhi Zhou, Linwen Liu, et al. "Functional Abnormality Associated With Tau Deposition in Alzheimer’s Disease – A Hybrid Positron Emission Tomography/MRI Study." Frontiers in Aging Neuroscience 13 (October 13, 2021). http://dx.doi.org/10.3389/fnagi.2021.758053.

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Objective: To investigate the characteristics of tau deposition and its impact on functional connectivity (FC) in Alzheimer’s disease (AD).Methods: Hybrid PET/MRI scans with [18F]-THK5317 and neuropsychological assessments were undertaken in 26 participants with AD and 19 healthy controls (HC). The standardized uptake value ratio (SUVR) of [18F]-THK5317 PET imaging was compared between the AD and HC groups. Significant clusters that revealed higher tau deposition in the AD group compared to the HC group were selected as regions of interest (ROI) for FC analysis. We evaluated the difference in
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Fu, Liping, Jinming Zhang, Kaixiang Zhou, et al. "In vivo imaging of tau deposition in Alzheimer’s disease using both [18F]-THK5317 and [18F]-S16: A pilot human study." Frontiers in Aging Neuroscience 14 (August 26, 2022). http://dx.doi.org/10.3389/fnagi.2022.994750.

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ObjectiveTo evaluate the effectiveness of a new tracer (S)-1-(4-(6-(dimethylamino)quinoxalin-2-yl)phenoxy)-3-fluoropropan-2-ol ([18F]-S16), in distinguishing patients with AD from HCs.MethodsPaired [18F]-S16 and [18F]-THK5317 scans were acquired in five patients with AD, six HCs, one subject with a semantic variant of primary progressive aphasia (sv-PPA) and one subject with probable progressive supranuclear palsy (PSP). Dynamic PET scanning was performed over 90 min after injection of the tracers. Standardized uptake values (SUV) and cortical-to-cerebellum standardized uptake value ratios (SU
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Chiotis, Konstantinos, Irina Savitcheva, Konstantinos Poulakis, et al. "[18F]THK5317 imaging as a tool for predicting prospective cognitive decline in Alzheimer’s disease." Molecular Psychiatry, July 3, 2020. http://dx.doi.org/10.1038/s41380-020-0815-4.

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