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1

Lilleker, James B., Richard Hodgson, Mark Roberts, et al. "[18F]Florbetapir positron emission tomography: identification of muscle amyloid in inclusion body myositis and differentiation from polymyositis." Annals of the Rheumatic Diseases 78, no. 5 (2019): 657–62. http://dx.doi.org/10.1136/annrheumdis-2018-214644.

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ObjectivesWith the tools available currently, confirming the diagnosis of inclusion body myositis (IBM) can be difficult. Many patients are initially misdiagnosed with polymyositis (PM). In this observational study at a UK adult neuromuscular centre, we investigated whether amyloid positron emission tomography could differentiate between IBM and PM.MethodsTen patients with IBM and six with PM underwent clinical review, [18F]florbetapir positron emission tomography and MRI of skeletal musculature. Differences in [18F]florbetapir standardised uptake value ratios in skeletal muscle regions of int
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B, Lilleker James, Hodgson Richard, Roberts Mark E, et al. "283 Quantifying muscle amyloid in inclusion body myositis using pet." Journal of Neurology, Neurosurgery & Psychiatry 89, no. 10 (2018): A42.3—A43. http://dx.doi.org/10.1136/jnnp-2018-abn.147.

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ObjectivesInclusion body myositis (IBM) shares some histopathological features with polymyositis (PM). Current investigations have low sensitivity for identification of amyloid deposits that are characteristic of IBM, contributing to frequent misdiagnosis. We compared muscle amyloid content, quantified using a novel positron emission tomography (PET) technique, in IBM and PM.MethodsTen cases with IBM and six controls with PM underwent clinical review, [18F]florbetapir PET/computed tomography, and magnetic resonance imaging (MRI) of whole-body skeletal musculature. [18F]florbetapir standardised
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Golla, Sandeep SV, Sander CJ Verfaillie, Ronald Boellaard, et al. "Quantification of [18F]florbetapir: A test–retest tracer kinetic modelling study." Journal of Cerebral Blood Flow & Metabolism 39, no. 11 (2018): 2172–80. http://dx.doi.org/10.1177/0271678x18783628.

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Accumulation of amyloid beta can be visualized using [18F]florbetapir positron emission tomography. The aim of this study was to identify the optimal model for quantifying [18F]florbetapir uptake and to assess test–retest reliability of corresponding outcome measures. Eight Alzheimer’s disease patients (age: 67 ± 6 years, Mini-Mental State Examination (MMSE): 23 ± 3) and eight controls (age: 63 ± 4 years, MMSE: 30 ± 0) were included. Ninety-minute dynamic positron emission tomography scans, together with arterial blood sampling, were acquired immediately following a bolus injection of 294 ± 32
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4

Carotenuto, Antonio, Beniamino Giordano, George Dervenoulas, et al. "[18F]Florbetapir PET/MR imaging to assess demyelination in multiple sclerosis." European Journal of Nuclear Medicine and Molecular Imaging 47, no. 2 (2019): 366–78. http://dx.doi.org/10.1007/s00259-019-04533-y.

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Abstract Purpose We evaluated myelin changes throughout the central nervous system in Multiple Sclerosis (MS) patients by using hybrid [18F]florbetapir PET-MR imaging. Methods We included 18 relapsing-remitting MS patients and 12 healthy controls. Each subject performed a hybrid [18F]florbetapir PET-MR and both a clinical and cognitive assessment. [18F]florbetapir binding was measured as distribution volume ratio (DVR), through the Logan graphical reference method and the supervised cluster analysis to extract a reference region, and standard uptake value (SUV) in the 70–90 min interval after
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5

Meng, Huanyu, Shuyu Zheng, Shaicun Yuan, et al. "Hybrid 18F-florbetapir PET/MRI for assessing myelin recovery in GFAP-A patients." Translational Neuroscience 13, no. 1 (2022): 120–24. http://dx.doi.org/10.1515/tnsci-2022-0223.

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Abstract Glial fibrillary acidic protein astrocytopathy (GFAP-A) is a rare autoimmune disease of the central nervous system that was newly reported in 2016. Previous studies have speculated that the pathological mechanism and clinical outcome of GFAP-A lie in the demyelination of the central nervous system, but due to the limitations of MR, this conclusion has not been further confirmed from the perspective of neuroimaging. A non-invasive, quantitative measurement of demyelination would be clinically valuable, given its critical role in mediating GFAP-A. Here, we report a case in which we use
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6

Raposo, Nicolas, Mélanie Planton, Patrice Péran, et al. "Florbetapir imaging in cerebral amyloid angiopathy-related hemorrhages." Neurology 89, no. 7 (2017): 697–704. http://dx.doi.org/10.1212/wnl.0000000000004228.

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Objective:To assess whether 18F-florbetapir, a PET amyloid tracer, could bind vascular amyloid in cerebral amyloid angiopathy (CAA) by comparing cortical florbetapir retention during the acute phase between patients with CAA-related lobar intracerebral hemorrhage (ICH) and patients with hypertension-related deep ICH.Methods:Patients with acute CAA-related lobar ICH were prospectively enrolled and compared with patients with deep ICH. 18F-florbetapir PET, brain MRI, and APOE genotype were obtained for all participants. Cortical florbetapir standard uptake value ratio (SUVr) was calculated with
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7

Tedeschi Dauar, Marina, Tharick Ali Pascoal, Joseph Therriault, et al. "Dynamic Amyloid and Metabolic Signatures of Delayed Recall Performance within the Clinical Spectrum of Alzheimer’s Disease." Brain Sciences 13, no. 2 (2023): 232. http://dx.doi.org/10.3390/brainsci13020232.

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Associations between pathophysiological events and cognitive measures provide insights regarding brain networks affected during the clinical progression of Alzheimer’s disease (AD). In this study, we assessed patients’ scores in two delayed episodic memory tests, and investigated their associations with regional amyloid deposition and brain metabolism across the clinical spectrum of AD. We assessed the clinical, neuropsychological, structural, and positron emission tomography (PET) baseline measures of participants from the Alzheimer’s Disease Neuroimaging Initiative. Subjects were classified
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8

Bailly, Matthieu, Maria Joao Santiago Ribeiro, Johny Vercouillie, et al. "18F-FDG and 18F-Florbetapir PET in Clinical Practice." Clinical Nuclear Medicine 40, no. 2 (2015): e111-e116. http://dx.doi.org/10.1097/rlu.0000000000000666.

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9

de Vries, Bart M., Tessa Timmers, Emma E. Wolters, et al. "Non-invasive Standardised Uptake Value for Verification of the Use of Previously Validated Reference Region for [18F]Flortaucipir and [18F]Florbetapir Brain PET Studies." Molecular Imaging and Biology 23, no. 4 (2021): 550–59. http://dx.doi.org/10.1007/s11307-020-01572-y.

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Abstract Purpose The simplified reference tissue model (SRTM) is commonly applied for the quantification of brain positron emission tomography (PET) studies, particularly because it avoids arterial cannulation. SRTM requires a validated reference region which is obtained by baseline-blocking or displacement studies. Once a reference region is validated, the use should be verified for each new subject. This verification normally requires volume of distribution (VT) of a reference region. However, performing dynamic scanning and arterial sampling is not always possible, specifically in elderly s
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Soffers, Frederik, Sarah Ceyssens, Wendi Buffet, Didier de Surgeloose, and Roeland Crols. "18F-Florbetapir PET in Primary Cerebral Amyloidoma." Clinical Nuclear Medicine 45, no. 10 (2020): 838–39. http://dx.doi.org/10.1097/rlu.0000000000003214.

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11

Asghar, Michael, Rainer Hinz, Karl Herholz, and Stephen F. Carter. "Dual-phase [18F]florbetapir in frontotemporal dementia." European Journal of Nuclear Medicine and Molecular Imaging 46, no. 2 (2018): 304–11. http://dx.doi.org/10.1007/s00259-018-4238-2.

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12

Yeo, Jing Ming, Briony Waddell, Zubair Khan, and Suvankar Pal. "A SYSTEMATIC REVIEW & META-ANALYSIS OF F-18-LABELLED AMYLOID IMAGING IN ALZHEIMER'S DISEASE." Journal of Neurology, Neurosurgery & Psychiatry 86, no. 11 (2015): e4.142-e4. http://dx.doi.org/10.1136/jnnp-2015-312379.51.

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IntroductionThere has been recent interest in the use of fluorine-18-labelled (18F) tracers in amyloid imaging as they have longer half-lives compared to 11C-labelled Pittsburgh compound-B (11C-PIB). This systematic review and meta-analysis aims to assess the sensitivity and specificity of 18F tracers florbetapir, florbetaben and flutemetamol in diagnosing Alzheimer's disease (AD).MethodsWe systematically searched MEDLINE and EMBASE for relevant studies published from January 1980 to March 2014. We pooled the studies comparing imaging findings in AD and normal controls (NC) in a meta-analysis,
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13

Lu, M., M. Pontecorvo, A. Siderowf, et al. "Prognostic value of 8F-Florbetapir scan: a 36-month follow up analysis using ADNI data." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 42, S1 (2015): S30. http://dx.doi.org/10.1017/cjn.2015.143.

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Background: The Alzheimer’s Disease Neuroimaging Initiative (ADNI) provides an opportunity to investigate the relationship between β-Amyloid neuropathology and patients’ long-term cognitive function change. We examined baseline 18F-florbetapir PET amyloid imaging status and 36-months’ change from baseline in cognitive performance in subjects with mild cognitive impairment (MCI). Method: The study included all ADNI subjects who underwent PET-imaging with 18F-florbetapir and had a clinical diagnosis of MCI at the visit closest to florbetapir imaging. β-Amyloid deposition was measured by florbeta
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14

Fakhry-Darian, Daniel, Neva Hiten Patel, Sairah Khan, et al. "Optimisation and usefulness of quantitative analysis of18F-florbetapir PET." British Journal of Radiology 92, no. 1101 (2019): 20181020. http://dx.doi.org/10.1259/bjr.20181020.

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Objectives:This study investigates the usefulness of quantitative SUVR thresholds on sub types of typical (type A) and atypical (non-type A) positive (Aβ+) and negative (Aβ-)18F-florbetapir scans and aims to optimise the thresholds.Methods:Clinical18F-florbetapir scans (n = 100) were categorised by sub type and visual reads were performed independently by three trained readers. Inter-reader agreement and reader-to-reference agreement were measured. Optimal SUVR thresholds were derived by ROC analysis and were compared with thresholds derived from a healthy control group and values from publish
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15

Therriault, Joseph, Kok Pin Ng, Tharick A. Pascoal, et al. "Anosognosia predicts default mode network hypometabolism and clinical progression to dementia." Neurology 90, no. 11 (2018): e932-e939. http://dx.doi.org/10.1212/wnl.0000000000005120.

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ObjectiveTo identify the pathophysiologic mechanisms and clinical significance of anosognosia for cognitive decline in mild cognitive impairment.MethodsWe stratified 468 patients with amnestic mild cognitive impairment into intact and impaired awareness groups, determined by the discrepancy between the patient and the informant score on the Everyday Cognition questionnaire. Voxel-based linear regression models evaluated the associations between self-awareness status and baseline β-amyloid load, measured by [18F]florbetapir, and the relationships between awareness status and regional brain gluc
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16

Skovronsky, Daniel. "Amyloid imaging with 18F-AV-45 (florbetapir F 18)." Neuroscience Research 71 (September 2011): e39. http://dx.doi.org/10.1016/j.neures.2011.07.173.

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17

Reimand, Juhan, Lyduine Collij, Philip Scheltens, Femke Bouwman та Rik Ossenkoppele. "Association of amyloid-β CSF/PET discordance and tau load 5 years later". Neurology 95, № 19 (2020): e2648-e2657. http://dx.doi.org/10.1212/wnl.0000000000010739.

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ObjectiveTo investigate the association between discordant β-amyloid (Aβ) PET and CSF biomarkers at baseline and the emergence of tau pathology 5 years later.MethodsWe included 730 Alzheimer's Disease Neuroimaging Initiative (ADNI) participants without dementia (282 cognitively normal, 448 mild cognitive impairment) with baseline [18F]florbetapir PET and CSF Aβ42 available. Aβ CSF/PET status was determined at baseline using established cutoffs. Longitudinal data were available for [18F]florbetapir (Aβ) PET (baseline to 4.3 ± 1.9 years), CSF (p)tau (baseline to 2.0 ± 0.1 years), cognition (base
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18

Landau, Susan M., Andy Horng, and William J. Jagust. "Memory decline accompanies subthreshold amyloid accumulation." Neurology 90, no. 17 (2018): e1452-e1460. http://dx.doi.org/10.1212/wnl.0000000000005354.

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ObjectiveExtensive cortical β-amyloid (Aβ positivity) has been linked to cognitive decline, but the clinical significance of elevations in Aβ within the negative range is unknown.MethodsWe examined amyloid and cognitive trajectories (memory, executive function) in 142 cognitively normal older individuals enrolled in the Alzheimer's Disease Neuroimaging Initiative who were Aβ-negative at baseline and who had at least 2 [18F]-florbetapir PET scans over 3.9 ± 1.4 years. We determined whether Aβ accumulation was associated with longitudinal changes in memory or executive function.ResultsAmong base
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19

Schmidt, Mark E., Luc Janssens, Diederik Moechars, et al. "Clinical evaluation of [18F] JNJ-64326067, a novel candidate PET tracer for the detection of tau pathology in Alzheimer’s disease." European Journal of Nuclear Medicine and Molecular Imaging 47, no. 13 (2020): 3176–85. http://dx.doi.org/10.1007/s00259-020-04880-1.

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Abstract Purpose The accumulation of misfolded tau is a common feature of several neurodegenerative disorders, with Alzheimer’s disease (AD) being the most common. Earlier we identified JNJ-64326067, a novel isoquinoline derivative with high affinity and selectivity for tau aggregates from human AD brain. We report the dosimetry of [18F] JNJ-64326067 and results of a proof-of-concept study comparing subjects with probable Alzheimer’s disease to age-matched healthy controls. Methods [18F] JNJ-64326067 PET scans were acquired for 90 min and then from 120 to 180 min in 5 participants with [18F]-f
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20

Trembath, L., M. Newell, and M. D. Devous. "Technical Considerations in Brain Amyloid PET Imaging with 18F-Florbetapir." Journal of Nuclear Medicine Technology 43, no. 3 (2015): 175–84. http://dx.doi.org/10.2967/jnmt.115.156679.

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21

Nakano, Masako, Tomomi Nakamura, Yasushi Takita, et al. "Radiation dosimetry and pharmacokinetics of florbetapir (18F) in Japanese subjects." Annals of Nuclear Medicine 33, no. 8 (2019): 639–45. http://dx.doi.org/10.1007/s12149-019-01366-5.

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22

García-González, P., R. Sánchez-Jurado, M. P. Cozar-Santiago, M. Ferrando-Beltrán, P. L. Pérez-Rodriguez, and J. Ferrer-Rebolleda. "Laryngeal and cardiac amyloidosis diagnosed by 18F-Florbetapir PET/CT." Revista Española de Medicina Nuclear e Imagen Molecular 36, no. 2 (2017): 135–36. http://dx.doi.org/10.1016/j.remn.2016.03.006.

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23

Hutton, Chloe, Jerome Declerck, Mark A. Mintun, Michael J. Pontecorvo, Michael D. Devous, and Abhinay D. Joshi. "Quantification of 18F-florbetapir PET: comparison of two analysis methods." European Journal of Nuclear Medicine and Molecular Imaging 42, no. 5 (2015): 725–32. http://dx.doi.org/10.1007/s00259-015-2988-7.

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Martínez-Valle, Fernando, Mercedes Gironella, Mar Riveiro-Barciela, and Carles Lorenzo-Bosquet. "Assessment of amyloid deposits by 18F-florbetapir positron emission tomography." European Journal of Nuclear Medicine and Molecular Imaging 42, no. 11 (2015): 1778–79. http://dx.doi.org/10.1007/s00259-015-3108-4.

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25

Siriprapa, Tossaporn, Tanyaluck Thientunyakit, and Juri Gelovani. "Amyloid PET Radiopharmaceuticals and Imaging for Clinical and Research Applications in Thailand." Siriraj Medical Journal 75, no. 9 (2023): 688–98. http://dx.doi.org/10.33192/smj.v75i9.263161.

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In the past two decades, the research community has focused on defining reliable molecular biomarkers for the early diagnosis of Alzheimer's disease (AD). Several PET radiopharmaceuticals have been developed and gained regulatory approval for the non-invasive detection of Aβ amyloid deposits in the brain. Nowadays, there are several PET imaging tracers available in Thailand for amyloid imaging including [11C]PiB, [18F]Florbetapir, and [18F]Florbetaben. This review provides a summary of commonly used amyloid PET radiopharmaceuticals, focusing on the available radiopharmaceuticals in Thailand an
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Seiffert, Alexander P., Adolfo Gómez-Grande, Alberto Villarejo-Galende, et al. "High Correlation of Static First-Minute-Frame (FMF) PET Imaging after 18F-Labeled Amyloid Tracer Injection with [18F]FDG PET Imaging." Sensors 21, no. 15 (2021): 5182. http://dx.doi.org/10.3390/s21155182.

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Dynamic early-phase PET images acquired with radiotracers binding to fibrillar amyloid-beta (Aβ) have shown to correlate with [18F]fluorodeoxyglucose (FDG) PET images and provide perfusion-like information. Perfusion information of static PET scans acquired during the first minute after radiotracer injection (FMF, first-minute-frame) is compared to [18F]FDG PET images. FMFs of 60 patients acquired with [18F]florbetapir (FBP), [18F]flutemetamol (FMM), and [18F]florbetaben (FBB) are compared to [18F]FDG PET images. Regional standardized uptake value ratios (SUVR) are directly compared and intrap
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Auvity, Sylvain, Matteo Tonietto, Fabien Caillé, et al. "Repurposing radiotracers for myelin imaging: a study comparing 18F-florbetaben, 18F-florbetapir, 18F-flutemetamol,11C-MeDAS, and 11C-PiB." European Journal of Nuclear Medicine and Molecular Imaging 47, no. 2 (2019): 490–501. http://dx.doi.org/10.1007/s00259-019-04516-z.

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28

Kobylecki, C., T. Langheinrich, R. Hinz, et al. "18F-Florbetapir PET in Patients with Frontotemporal Dementia and Alzheimer Disease." Journal of Nuclear Medicine 56, no. 3 (2015): 386–91. http://dx.doi.org/10.2967/jnumed.114.147454.

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29

Wagatsuma, Kei, Kenta Miwa, Muneyuki Sakata, Kenji Ishibashi, and Kenji Ishii. "Cross-validation of Quantitative Analytical Software Using 18F-florbetapir PET Imaging." Japanese Journal of Radiological Technology 77, no. 1 (2021): 32–40. http://dx.doi.org/10.6009/jjrt.2021_jsrt_77.1.32.

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30

Kudo, Masako, Hisashi Yonezawa, Toshihide Shibata, et al. "Imaging brain amyloid using the radioligand 18F-AV45 (Florbetapir F 18)." Cerebral Blood Flow and Metabolism (Japanese journal of cerebral blood flow and metabolism) 25, no. 2 (2014): 91–96. http://dx.doi.org/10.16977/cbfm.25.2_91.

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31

Mestre-Torres, Jaume, Carles Lorenzo-Bosquet, Gemma Cuberas-Borrós, et al. "Utility of the 18F-Florbetapir positron emission tomography in systemic amyloidosis." Amyloid 25, no. 2 (2018): 109–14. http://dx.doi.org/10.1080/13506129.2018.1467313.

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32

Mattsson, Niklas, Sebastian Palmqvist та Oskar Hansson. "P4-278: STAGING β-AMYLOID PATHOLOGY WITH 18F-FLORBETAPIR PET IMAGING". Alzheimer's & Dementia 15 (липень 2019): P1389—P1390. http://dx.doi.org/10.1016/j.jalz.2019.06.3947.

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33

Ben Bouallègue, Fayçal, Denis Mariano-Goulart, and Pierre Payoux. "Joint Assessment of Quantitative 18F-Florbetapir and 18F-FDG Regional Uptake Using Baseline Data from the ADNI." Journal of Alzheimer's Disease 62, no. 1 (2018): 399–408. http://dx.doi.org/10.3233/jad-170833.

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34

Newberg, A. B., S. E. Arnold, N. Wintering, B. W. Rovner, and A. Alavi. "Initial Clinical Comparison of 18F-Florbetapir and 18F-FDG PET in Patients with Alzheimer Disease and Controls." Journal of Nuclear Medicine 53, no. 6 (2012): 902–7. http://dx.doi.org/10.2967/jnumed.111.099606.

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35

Broski, Stephen M., Robert J. Spinner, Benjamin M. Howe, Angela Dispenzieri, and Geoffrey B. Johnson. "18F-Florbetapir and 18F-FDG PET/CT in Systemic Immunoglobulin Light Chain Amyloidosis Involving the Peripheral Nerves." Clinical Nuclear Medicine 41, no. 2 (2016): e115-e117. http://dx.doi.org/10.1097/rlu.0000000000000947.

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Beaufils, Emilie, Maria Joao-Ribeiro, Karl Mondon, et al. "P3-120: PET with 18F-AV-45 (florbetapir) in posterior cortical atrophy." Alzheimer's & Dementia 9 (July 2013): P597—P598. http://dx.doi.org/10.1016/j.jalz.2013.05.1191.

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37

Dorbala, Sharmila, Divya Vangala, James Semer, et al. "Imaging cardiac amyloidosis: a pilot study using 18F-florbetapir positron emission tomography." European Journal of Nuclear Medicine and Molecular Imaging 41, no. 9 (2014): 1652–62. http://dx.doi.org/10.1007/s00259-014-2787-6.

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38

Yamao, Tensho, Kenta Miwa, Yuta Kaneko, et al. "Deep Learning-Driven Estimation of Centiloid Scales from Amyloid PET Images with 11C-PiB and 18F-Labeled Tracers in Alzheimer’s Disease." Brain Sciences 14, no. 4 (2024): 406. http://dx.doi.org/10.3390/brainsci14040406.

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Background: Standard methods for deriving Centiloid scales from amyloid PET images are time-consuming and require considerable expert knowledge. We aimed to develop a deep learning method of automating Centiloid scale calculations from amyloid PET images with 11C-Pittsburgh Compound-B (PiB) tracer and assess its applicability to 18F-labeled tracers without retraining. Methods: We trained models on 231 11C-PiB amyloid PET images using a 50-layer 3D ResNet architecture. The models predicted the Centiloid scale, and accuracy was assessed using mean absolute error (MAE), linear regression analysis
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Blazhenets, Ganna, Yilong Ma, Arnd Sörensen, et al. "Predictive Value of 18F-Florbetapir and 18F-FDG PET for Conversion from Mild Cognitive Impairment to Alzheimer Dementia." Journal of Nuclear Medicine 61, no. 4 (2019): 597–603. http://dx.doi.org/10.2967/jnumed.119.230797.

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40

Chiotis, Konstantinos, Stephen F. Carter, Karim Farid, Irina Savitcheva, and Agneta Nordberg. "Amyloid PET in European and North American cohorts; and exploring age as a limit to clinical use of amyloid imaging." European Journal of Nuclear Medecine and Molecular Imaging 42, no. 10 (2015): 1492–506. https://doi.org/10.1007/s00259-015-3115-5.

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PURPOSE: Several radiotracers that bind to fibrillar amyloid-beta in the brain have been developed and used in various patient cohorts. This study aimed to investigate the comparability of two amyloid positron emission tomography (PET) tracers as well as examine how age affects the discriminative properties of amyloid PET imaging. METHODS: Fifty-one healthy controls (HCs), 72 patients with mild cognitive impairment (MCI) and 90 patients with Alzheimer's disease (AD) from a European cohort were scanned with [11C]Pittsburgh compound-B (PIB) and compared with an age-, sex- and disease severit
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41

Saint-Aubert, Laure, Mélanie Planton, Didier Hannequin та ін. "Amyloid Imaging with AV45 (18F-florbetapir) in a Cognitively Normal AβPP Duplication Carrier". Journal of Alzheimer's Disease 28, № 4 (2012): 877–83. http://dx.doi.org/10.3233/jad-2011-111598.

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42

Guillon, L., K. Strelnikov, L. Saint-Aubert, and P. Payoux. "Étude préliminaire sur la cross-corrélation cérébrale, utilisant le 18F-Florbetapir (+ Running poster)." Médecine Nucléaire 45, no. 4 (2021): 217. http://dx.doi.org/10.1016/j.mednuc.2021.06.090.

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43

Tateno, Amane, Takeshi Sakayori, Makoto Higuchi, et al. "Amyloid imaging with [18F]florbetapir in geriatric depression: early-onset versus late-onset." International Journal of Geriatric Psychiatry 30, no. 7 (2014): 720–28. http://dx.doi.org/10.1002/gps.4215.

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44

Seiffert, Alexander P., Adolfo Gómez-Grande, Eva Milara, et al. "Texture-Based Analysis of 18F-Labeled Amyloid PET Brain Images." Applied Sciences 11, no. 5 (2021): 1991. http://dx.doi.org/10.3390/app11051991.

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Amyloid positron emission tomography (PET) brain imaging with radiotracers like [18F]florbetapir (FBP) or [18F]flutemetamol (FMM) is frequently used for the diagnosis of Alzheimer’s disease. Quantitative analysis is usually performed with standardized uptake value ratios (SUVR), which are calculated by normalizing to a reference region. However, the reference region could present high variability in longitudinal studies. Texture features based on the grey-level co-occurrence matrix, also called Haralick features (HF), are evaluated in this study to discriminate between amyloid-positive and neg
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Hayashi, Kazutaka, Akiko Tachibana, Shusaku Tazawa, et al. "Preparation and stability of ethanol-free solution of [18F]florbetapir ([18F]AV-45) for positron emission tomography amyloid imaging." Journal of Labelled Compounds and Radiopharmaceuticals 56, no. 5 (2013): 295–300. http://dx.doi.org/10.1002/jlcr.3021.

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Barthélemy, Nicolas R., Balazs Toth, Paul T. Manser, et al. "Site-Specific Cerebrospinal Fluid Tau Hyperphosphorylation in Response to Alzheimer’s Disease Brain Pathology: Not All Tau Phospho-Sites are Hyperphosphorylated." Journal of Alzheimer's Disease 85, no. 1 (2022): 415–29. http://dx.doi.org/10.3233/jad-210677.

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Background: Understanding patterns of association between CSF phosphorylated tau (p-tau) species and clinical disease severity will aid Alzheimer’s disease (AD) diagnosis and treatment. Objective: To evaluate changes in tau phosphorylation ratios to brain imaging (amyloid PET, [18F]GTP1 PET, and MRI) and cognition across clinical stages of AD in two different cohorts. Methods: A mass spectrometry (MS)-based method was used to evaluate the relationship between p-tau/tau phosphorylation ratios on 11 sites in CSF and AD pathology measured by tau PET ([18F]GTP1) and amyloid PET ([18F]florbetapir o
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Guo, Tengfei, Susan M. Landau, and William J. Jagust. "Detecting earlier stages of amyloid deposition using PET in cognitively normal elderly adults." Neurology 94, no. 14 (2020): e1512-e1524. http://dx.doi.org/10.1212/wnl.0000000000009216.

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ObjectiveTo examine the feasibility of using cross-sectional PET to identify cognitive decliners among β-amyloid (Aβ)-negative cognitively normal (CN) elderly adults.MethodsWe determined the highest Aβ-affected region by ranking baseline and accumulation rates of florbetapir-PET regions in 355 CN elderly adults using 18F-florbetapir-PET from the Alzheimer's Disease Neuroimaging Initiative (ADNI). The banks of the superior temporal sulcus (BANKSSTS) were found as the highest Aβ-affected region, and Aβ positivity in this region was defined as above the lowest boundary of BANKSSTS standardized up
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Myoraku, Alison, Gregory Klein, Susan Landau, and Duygu Tosun. "Regional uptakes from early-frame amyloid PET and 18F-FDG PET scans are comparable independent of disease state." European Journal of Hybrid Imaging 6, no. 1 (2022). http://dx.doi.org/10.1186/s41824-021-00123-0.

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Abstract Purpose Positron emission tomography (PET) imaging with amyloid-beta (Aβ) tracers and 2-[18F] fluoro-2-Deoxy-d-glucose (18F-FDG) is extensively employed in Alzheimer’s disease (AD) studies as biomarkers of AD pathology and neurodegeneration. To reduce cost and additional burdens to the patient, early-frame uptake during Aβ PET scanning has been proposed as a surrogate measure of regional glucose metabolism. Considering the disease state specific impact of AD on neurovascular coupling, we investigated to what extent the information captured in the early frames of an Aβ-PET (18F-florbet
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Tuncel, Hayel, Denise Visser, Tessa Timmers, et al. "Head-to-head comparison of relative cerebral blood flow derived from dynamic [18F]florbetapir and [18F]flortaucipir PET in subjects with subjective cognitive decline." EJNMMI Research 13, no. 1 (2023). http://dx.doi.org/10.1186/s13550-023-01041-x.

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Abstract Background Dynamic PET imaging studies provide accurate estimates of specific binding, but also measure the relative tracer delivery (R1), which is a proxy for relative cerebral blood flow (rCBF). Recently, studies suggested that R1 obtained from different tracers could be used interchangeably and is irrespective of target tissue. However, the similarities or differences of R1 obtained from different PET tracers still require validation. Therefore, the goal of the current study was to compare R1 estimates, derived from dynamic [18F]florbetapir (amyloid) and [18F]flortaucipir (tau) PET
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Bouter, Yvonne, Robert M. Glasnek, Jannis M. Wenzel, and Caroline Bouter. "18F-FDG-PET and Multimodal Biomarker Integration: A Powerful Tool for Alzheimer’s Disease Diagnosis." Nuclear Medicine and Molecular Imaging, July 10, 2025. https://doi.org/10.1007/s13139-025-00932-2.

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Abstract An early, biomarker-based diagnosis of Alzheimer’s Disease (AD) is crucial, especially with the emerging availability of novel therapeutic options. However, the role of 18F-FDG-PET and its relationship to other PET and CSF biomarkers remains unclear. Therefore, the aim of this study was the evaluation of the role of 18F-FDG-PET in AD diagnosis and its relationship to other commonly used fluid and PET biomarkers and their individual and multimodal accuracy in AD diagnosis. We included n = 157 AD patients, n = 603 MCI patients, and n = 380 cognitively normal participants from the Alzhei
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