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Journal articles on the topic 'R-PK11195'

Author: Grafiati

Published: 2 June 2025

Last updated: 31 July 2025

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1

Bitker, Laurent, Nicolas Costes, Didier Le Bars, et al. "Noninvasive quantification of macrophagic lung recruitment during experimental ventilation-induced lung injury." Journal of Applied Physiology 127, no. 2 (2019): 546–58. http://dx.doi.org/10.1152/japplphysiol.00825.2018.

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Macrophagic lung infiltration is pivotal in the development of lung biotrauma because of ventilation-induced lung injury (VILI). We assessed the performance of [11C](R)-PK11195, a positron emission tomography (PET) radiotracer binding the translocator protein, to quantify macrophage lung recruitment during experimental VILI. Pigs ( n = 6) were mechanically ventilated under general anesthesia, using protective ventilation settings (baseline). Experimental VILI was performed by titrating tidal volume to reach a transpulmonary end-inspiratory pressure (∆PL) of 35–40 cmH2O. We acquired PET/compute

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2

Kobayashi, Masato, Teresa Jiang, Sanjay Telu, et al. "11C-DPA-713 has much greater specific binding to translocator protein 18 kDa (TSPO) in human brain than 11C-(R)-PK11195." Journal of Cerebral Blood Flow & Metabolism 38, no. 3 (2017): 393–403. http://dx.doi.org/10.1177/0271678x17699223.

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Positron emission tomography (PET) radioligands for translocator protein 18 kDa (TSPO) are widely used to measure neuroinflammation, but controversy exists whether second-generation radioligands are superior to the prototypical agent 11C-( R)-PK11195 in human imaging. This study sought to quantitatively measure the “signal to background” ratio (assessed as binding potential ( BPND)) of 11C-( R)-PK11195 compared to one of the most promising second-generation radioligands, 11C-DPA-713. Healthy subjects had dynamic PET scans and arterial blood measurements of radioligand after injection of either

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3

de Souza, Aline Morais, Caroline Cristiano Real, Mara de Souza Junqueira, et al. "Potential of [11C](R)-PK11195 PET Imaging for Evaluating Tumor Inflammation: A Murine Mammary Tumor Model." Pharmaceutics 14, no. 12 (2022): 2715. http://dx.doi.org/10.3390/pharmaceutics14122715.

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Background: Breast tumor inflammation is an immunological process that occurs mainly by mediation of Tumor-Associated Macrophages (TAM). Aiming for a specific measurement of tumor inflammation, the current study evaluated the potential of Positron Emission Tomography (PET) imaging with [11C](R)-PK11195 to evaluate tumor inflammation in a mammary tumor animal model. Methods: Female Balb/C mice were inoculated with 4T1 cells. The PET imaging with [11C](R)-PK11195 and [18F]FDG was acquired 3 days, 1 week, and 2 weeks after cell inoculation. Results: The [11C](R)-PK11195 tumor uptake increased fro

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Su, Zhangjie, Federico Roncaroli, Pascal F. Durrenberger, et al. "The 18-kDa Mitochondrial Translocator Protein in Human Gliomas: A 11C-(R)PK11195 PET Imaging and Neuropathology Study." Journal of Nuclear Medicine 56, no. 4 (2015): 512–7. https://doi.org/10.2967/jnumed.114.151621.

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The 18-kDa mitochondrial translocator protein (TSPO) is up-regulated in high grade astrocytomas and can be imaged by positron emission tomography (PET) using the selective radiotracer 11C-(R)PK11195. We investigated 11C-(R)PK11195 binding in human gliomas and its relationship with TSPO expression in tumor tissue and glioma associated microglia/macrophages within the tumors. METHODS: Twenty-two glioma patients underwent dynamic 11C-(R)PK11195 PET scans and perfusion MRI acquisition. Parametric maps of 11C-(R)PK11195 binding potential (BPND) were generated. Co-registered

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Boutin, Hervé, Katie Murray, Jesus Pradillo, et al. "[18F]GE-180: a novel TSPO radiotracer compared to [11C]PK11195 in a preclinical model of stroke." Eur J Nucl Med Mol Imaging 42, no. 3 (2014): 503–11. https://doi.org/10.1007/s00259-014-2939-8.

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PURPOSE: Neuroinflammation plays a critical role in various neuropathological conditions, and hence there is renewed interest in the translocator protein (TSPO) as a biomarker of microglial activation and macrophage infiltration in the brain. This is reflected in the large amount of research conducted seeking to replace the prototypical PET radiotracer 11C-R-PK11195 with a TSPO ligand with higher performance. Here we report the in vivo preclinical investigation of the novel TSPO tracer 18F-GE-180 in a rat model of stroke. METHODS: Focal cerebral ischaemia was induced in Wistar rats by 60-min o

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Alfaifi, B., E. Agushi, R. Hinz, A. Jackson, D. Lewis, and D. Coope. "P15.10.A USE OF DUAL TRACERS PET AS A PREDICTIVE BIOMARKER OF THE SITE OF RECURRENCE IN HIGH GRADE GLIOMA." Neuro-Oncology 25, Supplement_2 (2023): ii111—ii112. http://dx.doi.org/10.1093/neuonc/noad137.374.

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Abstract BACKGROUND High grade glioma has poor survival rate and tumour recurrence occurs despite current treatments. Positron emission tomography (PET) with [11C](R)PK11195 can evaluate translocator protein (TSPO) and [11C]methionine can assess amino acid transport. PET imaging might have the potential to detect tumour regions at baseline that will later develop as the site of recurrence. We compare TSPO measured using [11C](R)PK11195 and amino acid transport using [11C]methionine at baseline and investigate to what extend the two tracers can predict the site of tumour recurrence. MATERIAL AN

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7

Schuck, Phelipi Nunes, Caroline Machado Dartora, and Ana Maria Marques da Silva. "Geração de Imagens PET Estáticas com [11C]-(R)-PK11195: Definição do Intervalo Temporal." Revista Brasileira de Física Médica 11, no. 2 (2017): 25. http://dx.doi.org/10.29384/rbfm.2017.v11.n2.p25-29.

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O radiotraçador [11C]-(R)-PK11195 mostra afinidade com a microglia em imagens PET in vivo e vem sendo utilizado como indicador de doença inflamatória cerebral, como a esclerose múltipla (EM). Atualmente, não há consenso sobre o intervalo temporal adequado para gerar imagens PET estáticas com [11C]-(R)-PK11195. O objetivo deste trabalho é determinar o intervalo temporal mais adequado para a geração de imagens PET cerebrais estáticas adquiridas com [11C]-(R)-PK11195 para a quantificação. Foram geradas imagens PET estáticas com [11C]-(R)-PK11195 nos intervalos de: 0-60min, 5-20min, 5-30min, 10-60

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Gent, Yoony Y. J., Nazanin Ahmadi, Alexandre E. Voskuyl, et al. "Detection of Subclinical Synovitis with Macrophage Targeting and Positron Emission Tomography in Patients with Rheumatoid Arthritis without Clinical Arthritis." Journal of Rheumatology 41, no. 11 (2014): 2145–52. http://dx.doi.org/10.3899/jrheum.140059.

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Objective.To determine whether macrophage targeting by (R)-11C-PK11195 positron emission tomography (PET) can visualize subclinical joint inflammation in patients with rheumatoid arthritis (RA) without clinical arthritis during or after treatment, with flare as clinical outcome measure.Methods.(R)-11C-PK11195 PET and contrast-enhanced magnetic resonance imaging (MRI) of hands/wrists were performed in 29 patients with RA without clinical arthritis. (R)-11C-PK11195 PET uptake (semiquantitative score 0–3) in metacarpophalangeal, proximal interphalangeal, and wrist joints (i.e., 22 joints per pati

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Gerhard, Alexander. "In-vivo-Bildgebung "neuroinflammatorischer Veränderungen" mit PET; Grundlagen und Anwendung bei Parkinson-Syndromen In vivo Imaging of "Neuroinflammatory Changes" with PET; Background and Applications in Parkinsonian disorders." Nuklearmediziner 39, no. 04 (2016): 309–15. https://doi.org/10.1055/s-0042-113849.

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<strong>Zusammenfassung</strong>   Mikroglia sind residente immunkompetente Zellen des Gehirns, die durch unspezifische Schädigung aktiviert werden. Im aktivierten Zustand exprimieren sie das &bdquo;translocator protein 18 kD“ (TSPO) – früher peripherer Benzodiazepinrezeptor genannt, an welches hochspezifisch das Isoquinolin PK11195 bindet. Radioaktiv markiert kann das R-Enantiomer [<sup>11</sup>C] PK11195 als Ligand in der Positronenemissionstomografie (PET) genutzt werden und ermöglicht so die in-vivo-Darstellung &bdquo;aktiver“ neuroinflammatoris

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Kitade, Makoto, Hideaki Nakajima, Tetsuya Tsujikawa, et al. "Evaluation of (R)-[11C]PK11195 PET/MRI for Spinal Cord-Related Neuropathic Pain in Patients with Cervical Spinal Disorders." Journal of Clinical Medicine 12, no. 1 (2022): 116. http://dx.doi.org/10.3390/jcm12010116.

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Activated microglia are involved in secondary injury after acute spinal cord injury (SCI) and in development of spinal cord-related neuropathic pain (NeP). The aim of the study was to assess expression of translocator protein 18 kDa (TSPO) as an indicator of microglial activation and to investigate visualization of the dynamics of activated microglia in the injured spinal cord using PET imaging with (R)-[11C]PK11195, a specific ligand for TSPO. In SCI chimeric animal models, TSPO was expressed mainly in activated microglia. Accumulation of (R)-[3H]PK11195 was confirmed in autoradiography and i

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11

Rapic, Sara, Heiko Backes, Thomas Viel, et al. "Imaging microglial activation and glucose consumption in a mouse model of Alzheimer's disease." Neurobiology of Aging 34, no. 11 (2012): 351–4. https://doi.org/10.1016/j.neurobiolaging.2012.04.016.

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In Alzheimer’s disease (AD), persistent microglial activation as sign of chronic neuroinflammation contributes to disease progression. Our study aimed to in vivo visualize and quantify microglial activation in 13- to 15-month-old AD mice using [11C]-(R)-PK11195 and positron emission tomography (PET). We attempted to modulate neuroinflammation by subjecting the animals to an anti-inflammatory treatment with pioglitazone (5-weeks’ treatment, 5-week wash-out period). [11C]-(R)-PK11195 distribution volume values in AD mice were significantly higher compared with con

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Yokokura, Masamichi, Tatsuhiro Terada, Tomoyasu Bunai, et al. "Depiction of microglial activation in aging and dementia: Positron emission tomography with [11C]DPA713 versus [11C](R)PK11195." Journal of Cerebral Blood Flow & Metabolism 37, no. 3 (2016): 877–89. http://dx.doi.org/10.1177/0271678x16646788.

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The presence of activated microglia in the brains of healthy elderly people is a matter of debate. We aimed to clarify the degree of microglial activation in aging and dementia as revealed by different tracers by comparing the binding potential (BPND) in various brain regions using a first-generation translocator protein (TSPO) tracer [11C]( R)PK11195 and a second-generation tracer [11C]DPA713. The BPND levels, estimated using simplified reference tissue models, were compared among healthy young and elderly individuals and patients with Alzheimer’s disease (AD) and were correlated with clinica

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Kropholler, Marc A., Ronald Boellaard, Alie Schuitemaker, et al. "Development of a Tracer Kinetic Plasma Input Model for (R)-[11C]PK11195 Brain Studies." Journal of Cerebral Blood Flow & Metabolism 25, no. 7 (2005): 842–51. http://dx.doi.org/10.1038/sj.jcbfm.9600092.

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(R)-[11C]PK11195 ([1-(2-chlorophenyl)- N-methyl- N-(1-methylpropyl]-3-isoquinoline carboxamide) is a ligand for the peripheral benzodiazepine receptor, which, in the brain, is mainly expressed on activated microglia. Using both clinical studies and Monte Carlo simulations, the aim of this study was to determine which tracer kinetic plasma input model best describes (R)-[11C]PK11195 kinetics. Dynamic positron emission tomography (PET) scans were performed on 13 subjects while radioactivity in arterial blood was monitored online. Discrete blood samples were taken to generate a metabolite correct

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14

Schuitemaker, Alie, Bart NM van Berckel, Marc A. Kropholler, et al. "Evaluation of Methods for Generating Parametric (R)-[11C]PK11195 Binding Images." Journal of Cerebral Blood Flow & Metabolism 27, no. 9 (2007): 1603–15. http://dx.doi.org/10.1038/sj.jcbfm.9600459.

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Activated microglia can be visualised using ( R)-[11C]PK11195 (1-[2-chlorophenyl]- N-methyl- N-[1-methyl-propyl]-3-isoquinoline carboxamide) and positron emission tomography (PET). In previous studies, various methods have been used to quantify ( R)-[11C]PK11195 binding. The purpose of this study was to determine which parametric method would be best suited for quantifying ( R)-[11C]PK11195 binding at the voxel level. Dynamic ( R)-[11C]PK11195 scans with arterial blood sampling were performed in 20 healthy and 9 Alzheimer's disease subjects. Parametric images of both volume of distribution ( V

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15

Myers, R., R. B. Banati, T. Jones, and V. J. Cunningham. "Quantification of [11C](R)-PK11195 in Clinical PET." NeuroImage 7, no. 4 (1998): A37. http://dx.doi.org/10.1016/s1053-8119(18)31906-2.

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16

Su, Zhangjie, Karl Herholz, Alexander Gerhard, et al. "[(11)C]-(R)PK11195 tracer kinetics in the brain of glioma patients and a comparison of two referencing approaches." European Journal of Nuclear Medicine and Molecular Imaging 40, no. 9 (2013): 1406–19. https://doi.org/10.1007/s00259-013-2447-2.

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PURPOSE: Translocator protein (TSPO) is a biomarker of neuroinflammation that can be imaged by PET using [¹¹C]-(R)PK11195. We sought to characterize the [¹¹C]-(R)PK11195 kinetics in gliomas of different histotypes and grades, and to compare two reference tissue input functions (supervised cluster analysis versus cerebellar grey matter) for the estimation of [¹¹C]-(R)PK11195 binding in gliomas and surrounding brain structures. METHODS: Twenty-three glioma patients and ten age-matched controls underwent structural MRI and dynamic [¹¹C]-(R)PK11195

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Hardwick, Matthew J., Ming-Kai Chen, Kwamena Baidoo, Martin G. Pomper, and Tomás R. Guilarte. "In Vivo Imaging of Peripheral Benzodiazepine Receptors in Mouse Lungs: A Biomarker of Inflammation." Molecular Imaging 4, no. 4 (2005): 7290.2005.05133. http://dx.doi.org/10.2310/7290.2005.05133.

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The ability to visualize the immune response with radioligands targeted to immune cells will enhance our understanding of cellular responses in inflammatory diseases. Peripheral benzodiazepine receptors (PBR) are present in monocytes and neutrophils as well as in lung tissue. We used lipopolysaccharide (LPS) as a model of inflammation to assess whether the PBR could be used as a noninvasive marker of inflammation in the lungs. Planar imaging of mice administrated 10 or 30 mg/kg LPS showed increased [123I]-( R)-PK11195 radioactivity in the thorax 2 days after LPS treatment relative to control.

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Rizzo, Gaia, Mattia Veronese, Matteo Tonietto, et al. "Generalization of endothelial modelling of TSPO PET imaging: Considerations on tracer affinities." Journal of Cerebral Blood Flow & Metabolism 39, no. 5 (2017): 874–85. http://dx.doi.org/10.1177/0271678x17742004.

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The 18 kDa translocator protein (TSPO) is a marker of microglia activation and the main target of positron emission tomography (PET) ligands for neuroinflammation. Previous works showed that accounting for TSPO endothelial binding improves PET quantification for [11C]PBR28, [18F]DPA714 and [11C]-R-PK11195. It is still unclear, however, whether the vascular signal is tracer-dependent. This work aims to explore the relationship between the TSPO vascular and tissue components for PET tracers with varying affinity, also assessing the impact of affinity towards the differentiability amongst kinetic

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Molthoff, Carla F. M., Hedy Folkersma, Jessica C. Foster-Dingley, et al. "Combined microdialysis and longitudinal (R)-[11C]PK11195 PET study." NeuroImage 52 (August 2010): S35. http://dx.doi.org/10.1016/j.neuroimage.2010.04.217.

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Kropholler, M. A., R. Boellaard, E. H. Elzinga, et al. "Quantification of (R)-[11C]PK11195 binding in rheumatoid arthritis." European Journal of Nuclear Medicine and Molecular Imaging 36, no. 4 (2008): 624–31. http://dx.doi.org/10.1007/s00259-008-0987-7.

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Yankam Njiwa, J., N. Costes, C. Bouillot, et al. "Quantitative longitudinal imaging of activated microglia as a marker of inflammation in the pilocarpine rat model of epilepsy using [11C]-(R)-PK11195 PET and MRI." Journal of Cerebral Blood Flow & Metabolism 37, no. 4 (2016): 1251–63. http://dx.doi.org/10.1177/0271678x16653615.

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Inflammation may play a role in the development of epilepsy after brain insults. [11C]-( R)-PK11195 binds to TSPO, expressed by activated microglia. We quantified [11C]-( R)-PK11195 binding during epileptogenesis after pilocarpine-induced status epilepticus (SE), a model of temporal lobe epilepsy. Nine male rats were studied thrice (D0-1, D0 + 6, D0 + 35, D0 = SE induction). In the same session, 7T T2-weighted images and DTI for mean diffusivity (MD) and fractional anisotropy (FA) maps were acquired, followed by dynamic PET/CT. On D0 + 35, femoral arterial blood was sampled for rat-specific me

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Mantovani, Dimitri B. A., Milena S. Pitombeira, Phelipi N. Schuck, et al. "Evaluation of Non-Invasive Methods for (R)-[11C]PK11195 PET Image Quantification in Multiple Sclerosis." Journal of Imaging 10, no. 2 (2024): 39. http://dx.doi.org/10.3390/jimaging10020039.

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This study aims to evaluate non-invasive PET quantification methods for (R)-[11C]PK11195 uptake measurement in multiple sclerosis (MS) patients and healthy controls (HC) in comparison with arterial input function (AIF) using dynamic (R)-[11C]PK11195 PET and magnetic resonance images. The total volume of distribution (VT) and distribution volume ratio (DVR) were measured in the gray matter, white matter, caudate nucleus, putamen, pallidum, thalamus, cerebellum, and brainstem using AIF, the image-derived input function (IDIF) from the carotid arteries, and pseudo-reference regions from supervise

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Narciso, Lucas Diovani Lopes, Phelipi Nunes Schuck, Caroline Machado Dartora, Cristina Sebastião Matushita, Jefferson Becker, and Ana Maria Marques da Silva. "Semiquantification Study of [11C]-(R)-PK11195 PET Brain Images in Multiple Sclerosis." Revista Brasileira de Física Médica 10, no. 2 (2016): 39. http://dx.doi.org/10.29384/rbfm.2016.v10.n2.p39-43.

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PET brain images with [11C]-(R)-PK11195 are being widely used to visualize microglial activation in vivo in neurodegenerative diseases, such as multiple sclerosis (MS). The aim of this study is to investigate the uptake behavior in juxtacortical and periventricular regions of [11C]-(R)-PK11195 PET brain images reformatted in different time intervals by applying three methods, seeking method and time interval that significantly differentiate MS patients from healthy controls. Semiquantitative SUV and SUVR methods were applied to PET images from different time intervals acquired from 10 patients

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van, der Doef Thalia F., Witte Lot D. de, Arjen L. Sutterland, et al. "In vivo (R)-[11C]PK11195 PET imaging of 18kDa translocator protein in recent onset psychosis." NPJ Schizophrenia 2 (August 31, 2016): 16031. https://doi.org/10.1038/npjschz.2016.31.

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Evidence is accumulating that immune dysfunction is involved in the pathophysiology of schizophrenia. It has been hypothesized that microglia activation is present in patients with schizophrenia. Various <em>in vivo</em> and post-mortem studies have investigated this hypothesis, but as yet with inconclusive results. Microglia activation is associated with elevations in 18 kDa translocator protein (TSPO) levels, which can be measured with the positron emission tomography (PET) tracer <em>(R)</em>-[<sup>11</sup>C]PK11195. The purpose of the present study was to investigate microglia activ

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Seo, Seongho, Ye-Ha Jung, Dasom Lee, et al. "Abnormal neuroinflammation in fibromyalgia and CRPS using [11C]-(R)-PK11195 PET." PLOS ONE 16, no. 2 (2021): e0246152. http://dx.doi.org/10.1371/journal.pone.0246152.

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Purpose Fibromyalgia (FM) and complex regional pain syndrome (CRPS) share many pathological mechanisms related to chronic pain and neuroinflammation, which may contribute to the multifactorial pathological mechanisms in both FM and CRPS. The aim of this study was to assess neuroinflammation in FM patients compared with that in patients with CRPS and healthy controls. Methods Neuroinflammation was measured as the distribution volume ratio (DVR) of [11C]-(R)-PK11195 positron emission tomography (PET) in 12 FM patients, 11 patients with CRPS and 15 healthy controls. Results Neuroinflammation in F

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Sridharan, Sujata, Francois-Xavier Lepelletier, William Trigg, et al. "Comparative Evaluation of Three TSPO PET Radiotracers in a LPS-Induced Model of Mild Neuroinflammation in Rats." Molecular Imaging & Biology 19 (August 1, 2016): 77–89. https://doi.org/10.1007/s11307-016-0984-3.

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PURPOSE: Over the past 20 years, neuroinflammation (NI) has increasingly been recognised as having an important role in  many neurodegenerative diseases, including Alzheimer's disease. As such, being able to image NI non-invasively in patients is critical to monitor pathological processes and potential therapies targeting neuroinflammation. The translocator protein (TSPO) has proven a reliable NI biomarker for positron emission tomography (PET) imaging. However, if TSPO imaging in acute conditions such as stroke provides strong and reliable signals, TSPO imaging in neurodegenerat

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Dickens, Alex M., Susanne Vainio, Päivi Marjamäki, et al. "Detection of Microglial Activation in an Acute Model of Neuroinflammation Using PET and Radiotracers 11C-(R)-PK11195 and 18F-GE-180." J Nucl Med. 55, no. 3 (2014): 466–72. https://doi.org/10.2967/jnumed.113.125625.

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It remains unclear how different translocator protein (TSPO) ligands reflect the spatial extent of astrocyte or microglial activation in various neuroinflammatory conditions. Here, we use a reproducible lipopolysaccharide (LPS)-induced model of acute central nervous system inflammation to compare the binding performance of a new TSPO ligand (18)F-GE-180 with (11)C-(R)-PK11195. Using immunohistochemistry, we also explore the ability of the TSPO ligands to detect activated microglial cells and astrocytes. METHODS: Lewis rats (n = 30) were microinjected with LPS (1 or 10 μg) or saline (1 μL

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Raijmakers, Ruud, Megan Roerink, Stephan Keijmel, et al. "No Signs of Neuroinflammation in Women With Chronic Fatigue Syndrome or Q Fever Fatigue Syndrome Using the TSPO Ligand [¹¹C]-PK11195." Neurology - Neuroimmunology Neuroinflammation 9, no. 1 (2021): e1113. http://dx.doi.org/10.1212/nxi.0000000000001113.

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Background and ObjectivesThe pathophysiology of chronic fatigue syndrome (CFS) and Q fever fatigue syndrome (QFS) remains elusive. Recent data suggest a role for neuroinflammation as defined by increased expression of translocator protein (TSPO). In the present study, we investigated whether there are signs of neuroinflammation in female patients with CFS and QFS compared with healthy women, using PET with the TSPO ligand 11C-(R)-(2-chlorophenyl)-N-methyl-N-(1-methylpropyl)-3-isoquinoline-carbox-amide ([11C]-PK11195).MethodsThe study population consisted of patients with CFS (n = 9), patients

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Tondo, Giacomo, Cecilia Boccalini, Silvia Paola Caminiti, et al. "Brain Metabolism and Microglia Activation in Mild Cognitive Impairment: A Combined [18F]FDG and [11C]-(R)-PK11195 PET Study." Journal of Alzheimer's Disease 80, no. 1 (2021): 433–45. http://dx.doi.org/10.3233/jad-201351.

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Background: Mild cognitive impairment (MCI) is a transitional condition between normal cognition and dementia. [18F]FDG-PET reveals brain hypometabolism patterns reflecting neuronal/synaptic dysfunction, already in the prodromal MCI phase. Activated microglia is part of the pathogenetic processes leading to neurodegeneration. Objective: Using [11C]-(R)-PK11195 and [18F]FDG-PET, we aimed to in vivo investigate the presence of microglial activation, and the relationship with brain glucose metabolism, in single MCI subjects. Methods: Eight MCI subjects underwent both [18F]FDG-PET and [11C]-(R)-PK

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Iaccarino, Leonardo, Luca Presotto, Valentino Bettinardi, et al. "An in vivo 11C-PK PET study of microglia activation in Fatal Familial Insomnia." Annals of Clinical and Translational Neurology 5, no. 1 (2017): 11–18. https://doi.org/10.1002/acn3.498.

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Abstract Objective: Postmortem studies reported significant microglia activation in association with neuronal apoptosis in Fatal Familial Insomnia (FFI), indicating a specific glial response, but negative evidence also exists. An in vivo study of local immune responses over FFI natural course may contribute to the understanding of the underlying pathogenesis. Methods: We included eight presymptomatic subjects (mean ± SD age:44.13 ± 3.83 years) carrying the pathogenic D178N-129<sup>met</sup> FFI mutation, one symptomatic patient (male, 45 yrs. ol

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Kropholler, Marc A., Bart N. M. van Berckel, Alie Schuitemaker, et al. "Evaluation of reference tissue models for analysing [11C](R)-PK11195 studies." Journal of Cerebral Blood Flow & Metabolism 25, no. 1_suppl (2005): S642. http://dx.doi.org/10.1038/sj.jcbfm.9591524.0642.

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Visi, Eszter, Rainer Hinz, Martin Punter, Arshad Majid, Alexander Gerhard, and Karl Herholz. "Positron emission tomography to image cerebral neuroinflammation in ischaemic stroke: a pilot study." Efficacy and Mechanism Evaluation 7, no. 1 (2020): 1–26. http://dx.doi.org/10.3310/eme07010.

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Background Activated microglia play a complex role in neuroinflammation associated with acute ischaemic stroke. As a potential target for anti-inflammatory therapy, it is crucial to understand the association between intensity, extent and the clinical outcome of a stroke. The 18-kDa translocator protein is a marker of cerebral microglial activation and of macrophage infiltration after damage to the brain. It can be imaged by positron emission tomography. Therefore, the recently developed radiopharmaceutical [18F]-GE180 was used in patients after a mild to moderate stroke and compared with [11C

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Kim, *Jong-Hoon, Yo-Han Joo, Jeong-Hee Kim, and Young-Don Son. "ALTERED PATTERNS OF ASSOCIATION BETWEEN TSPO BINDING AND MGLUR5 AVAILABILITY IN VIVO IN DRUG-NAIVE PATIENTS WITH MAJOR DEPRESSIVE DISORDER: A PRELIMINARY DUAL-TRACER PET STUDY." International Journal of Neuropsychopharmacology 28, Supplement_1 (2025): i137—i138. https://doi.org/10.1093/ijnp/pyae059.238.

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Abstract Background Based on the monoamine theory of major depressive disorder (MDD), symptoms are derived from a deficiency or imbalance in monoaminergic neurotransmission. The limitation of such a model (1) may highlight the need for alternative neurobiological constructs. Accumulating data indicate that neuroinflammation and its interactions with glutamatergic signaling may present a compelling alternative model for understanding the pathophysiology of MDD and its therapeutic approaches (2-4); however, the patterns of interregional correlations between neuroinflammation and glutamatergic si

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Chandrupatla, Durga M. S. H., Karin Weijers, Yoony Y. J. Gent, et al. "Sustained Macrophage Infiltration upon Multiple Intra-Articular Injections: An Improved Rat Model of Rheumatoid Arthritis for PET Guided Therapy Evaluation." BioMed Research International 2015 (2015): 1–11. http://dx.doi.org/10.1155/2015/509295.

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To widen the therapeutic window for PET guided evaluation of novel anti-RA agents, modifications were made in a rat model of rheumatoid arthritis (RA). Arthritis was induced in the right knee of Wistar rats with repeated boosting to prolong articular inflammation. The contralateral knee served as control. After immunization with methylated bovine serum albumin (mBSA) in complete Freund’s adjuvant and custom Bordetella pertussis antigen, one or more intra-articular (i.a.) mBSA injections were given over time in the right knee. Serum anti-mBSA antibodies, DTH response, knee thickness, motion, an

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Agushi, E., D. Coope, R. Hinz, A. Jackson, and F. Roncaroli. "P04.01 [11C]-(R)PK11195 PET imaging and Dynamic MRI in Transforming Gliomas." Neuro-Oncology 19, suppl_3 (2017): iii39. http://dx.doi.org/10.1093/neuonc/nox036.141.

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Gerhard, A., R. B. Banati, G. B. Goerres, et al. "[11C](R)-PK11195 PET imaging of microglial activation in multiple system atrophy." Neurology 61, no. 5 (2003): 686–89. http://dx.doi.org/10.1212/01.wnl.0000078192.95645.e6.

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Hunter, H. J. A., R. Hinz, A. Gerhard, et al. "Brain inflammation and psoriasis: a [11C]-(R)-PK11195 positron emission tomography study." British Journal of Dermatology 175, no. 5 (2016): 1082–84. http://dx.doi.org/10.1111/bjd.13788.

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van Berckel, Bart N. M., M. G. Bossong, R. Boellaard, et al. "Microglia activation in recent onset schizophrenia: A quantitative (R)-[11C]PK11195 study." NeuroImage 41 (January 2008): T119. http://dx.doi.org/10.1016/j.neuroimage.2008.04.087.

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Haarman, Bartholomeus C. M. (Benno), Rixt F. Riemersma-Van der Lek, Jan Cees de Groot, et al. "Neuroinflammation in bipolar disorder – A [11C]-(R)-PK11195 positron emission tomography study." Brain, Behavior, and Immunity 40 (August 2014): 219–25. http://dx.doi.org/10.1016/j.bbi.2014.03.016.

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van Berckel, Bart N. M., Ronald Boellaard, Marc A. Kropholler, et al. "Assessment of microglia activation in schizophrenia using [11C](R)-PK11195 and PET." Journal of Cerebral Blood Flow & Metabolism 25, no. 1_suppl (2005): S391. http://dx.doi.org/10.1038/sj.jcbfm.9591524.0391.

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Hammoud, Dima A., Christopher J. Endres, Ankit R. Chander, et al. "Imaging glial cell activation with [11C]-R-PK11195 in patients with AIDS." Journal of Neurovirology 11, no. 4 (2005): 346–55. http://dx.doi.org/10.1080/13550280500187351.

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Rissanen, Eero, Jouni Tuisku, Tero Vahlberg, et al. "Microglial activation, white matter tract damage, and disability in MS." Neurology - Neuroimmunology Neuroinflammation 5, no. 3 (2018): e443. http://dx.doi.org/10.1212/nxi.0000000000000443.

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ObjectiveTo investigate the relationship of in vivo microglial activation to clinical and MRI parameters in MS.MethodsPatients with secondary progressive MS (n = 10) or relapsing-remitting MS (n = 10) and age-matched healthy controls (n = 17) were studied. Microglial activation was measured using PET and radioligand [11C](R)-PK11195. Clinical assessment and structural and quantitative MRI including diffusion tensor imaging (DTI) were performed for comparison.Results[11C](R)-PK11195 binding was significantly higher in the normal-appearing white matter (NAWM) of patients with secondary progressi

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Cumming, Paul, Bjorn Burgher, Omkar Patkar, et al. "Sifting through the surfeit of neuroinflammation tracers." Journal of Cerebral Blood Flow & Metabolism 38, no. 2 (2017): 204–24. http://dx.doi.org/10.1177/0271678x17748786.

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The first phase of molecular brain imaging of microglial activation in neuroinflammatory conditions began some 20 years ago with the introduction of [11C]-( R)-PK11195, the prototype isoquinoline ligand for translocator protein (18 kDa) (TSPO). Investigations by positron emission tomography (PET) revealed microgliosis in numerous brain diseases, despite the rather low specific binding signal imparted by [11C]-( R)-PK11195. There has since been enormous expansion of the repertoire of TSPO tracers, many with higher specific binding, albeit complicated by allelic dependence of the affinity. Howev

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Yaqub, Maqsood, Bart NM van Berckel, Alie Schuitemaker, et al. "Optimization of Supervised Cluster Analysis for Extracting Reference Tissue Input Curves in (R)-[11C]PK11195 Brain PET Studies." Journal of Cerebral Blood Flow & Metabolism 32, no. 8 (2012): 1600–1608. http://dx.doi.org/10.1038/jcbfm.2012.59.

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Performance of two supervised cluster analysis (SVCA) algorithms for extracting reference tissue curves was evaluated to improve quantification of dynamic (R)-[11C]PK11195 brain positron emission tomography (PET) studies. Reference tissues were extracted from images using both a manually defined cerebellum and SVCA algorithms based on either four (SVCA4) or six (SVCA6) kinetic classes. Data from controls, mild cognitive impairment patients, and patients with Alzheimer's disease were analyzed using various kinetic models including plasma input, the simplified reference tissue model (RPM) and RP

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Verweij, N. J. F., M. Ter Wee, J. De Jongh, et al. "SAT0551 WHOLE BODY MACROPHAGE PET IMAGING THAT INCLUDES THE FEET CAN PROVIDE ADDITIONAL INFORMATION TO CLINICAL ASSESSMENT IN PATIENTS WITH EARLY RHEUMATOID ARTHRITIS." Annals of the Rheumatic Diseases 79, Suppl 1 (2020): 1233.2–1233. http://dx.doi.org/10.1136/annrheumdis-2020-eular.4380.

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Background:Clinical assessment of arthritis is the cornerstone in the diagnosis and treatment of rheumatoid arthritis (RA). Nevertheless, reliable determination of (sub)clinical arthritis can be difficult, especially in the feet. Advanced imaging techniques may contribute to early diagnosis and therapy monitoring through sensitive detection and (quantitative) monitoring of synovitis. Previously, it has been demonstrated that macrophage imaging using (R)-[11C]PK11195 positron emission tomography (PET) allows for highly sensitive and specific imaging of RA disease activity in the hands.(1,2)Whol

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Sucksdorff, Marcus, Eero Rissanen, Jouni Tuisku, et al. "Evaluation of the Effect of Fingolimod Treatment on Microglial Activation Using Serial PET Imaging in Multiple Sclerosis." Journal of Nuclear Medecine 58, no. 10 (2017): 1646–51. https://doi.org/10.2967/jnumed.116.183020.

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<strong>Abstract</strong> Traditionally, multiple sclerosis (MS) has been considered a white matter disease with focal inflammatory lesions. It is, however, becoming clear that significant pathology, such as microglial activation, also takes place outside the plaque areas, that is, in areas of normal-appearing white matter (NAWM) and gray matter (GM). Microglial activation can be detected in vivo using 18-kDa translocator protein (TSPO)-binding radioligands and PET. It is unknown whether fingolimod affects microglial activation in MS. The aim of this study was to investigate whether serial PET

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Lamare, F., R. Hinz, O. Gaemperli, et al. "Detection and Quantification of Large-Vessel Inflammation with 11C-(R)-PK11195 PET/CT." Journal of Nuclear Medicine 52, no. 1 (2010): 33–39. http://dx.doi.org/10.2967/jnumed.110.079038.

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Folkersma, H., R. Boellaard, M. Yaqub, et al. "Widespread and Prolonged Increase in (R)-11C-PK11195 Binding After Traumatic Brain Injury." Journal of Nuclear Medicine 52, no. 8 (2011): 1235–39. http://dx.doi.org/10.2967/jnumed.110.084061.

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Goerres, Gerhard W., Thomas Revesz, John Duncan, and Richard B. Banati. "Imaging Cerebral Vasculitis in Refractory Epilepsy Using [11C] (R)-PK11195 Positron Emission Tomography." American Journal of Roentgenology 176, no. 4 (2001): 1016–18. http://dx.doi.org/10.2214/ajr.176.4.1761016.

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Jeon, So Yeon, Seongho Seo, Jae Sung Lee, et al. "[11C]-(R)-PK11195 positron emission tomography in patients with complex regional pain syndrome." Medicine 96, no. 1 (2017): e5735. http://dx.doi.org/10.1097/md.0000000000005735.

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