Academic literature on the topic 'THK5117'

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Journal articles on the topic "THK5117"

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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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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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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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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