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Journal articles on the topic '11C-Pittsburgh compound B'

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Published: 2 June 2025

Last updated: 31 July 2025

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1

Ni, Ruiqing, Per-Göran Gillberg, Assar Bergfors, Amelia Marutle, and Agneta Nordberg. "Amyloid tracers detect multple binding sites in Alzheimer´s disease brain tissue." Brain 136, no. 7 (2013): 2217–27. https://doi.org/10.1093/brain/awt142.

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Imaging fibrillar amyloid-β deposition in the human brain <em>in vivo</em> by positron emission tomography has improved our understanding of the time course of amyloid-β pathology in Alzheimer’s disease. The most widely used amyloid-β imaging tracer so far is 11C-Pittsburgh compound B, a thioflavin derivative but other 11C- and 18F-labelled amyloid-β tracers have been studied in patients with Alzheimer's disease and cognitively normal control subjects. However, it has not yet been established whether different amyloid tracers bind to ident

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Lee, J. H., S. H. Kim, G. H. Kim, et al. "Identification of pure subcortical vascular dementia using 11C-Pittsburgh compound B." Neurology 77, no. 1 (2011): 18–25. http://dx.doi.org/10.1212/wnl.0b013e318221acee.

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Rodriguez-Vieitez, Elena, Laure Saint-Aubert, Stephen F. Carter, et al. "Diverging longitudinal changes in astrocytosis and amyloid PET in autosomal dominant Alzheimer's disease." Brain 139 (January 26, 2016): 922–36. https://doi.org/10.1093/brain/awv404.

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Alzheimer’s disease is a multifactorial dementia disorder characterized by early amyloid-b, tau deposition, glial activation and neurodegeneration, where the interrelationships between the different pathophysiological events are not yet well characterized. In this study, longitudinal multitracer positron emission tomography imaging of individuals with autosomal dominant or sporadic Alzheimer’s disease was used to quantify the changes in regional distribution of brain astrocytosis (tracer 11C-deuterium-L-deprenyl), fibrillar amyloid-b plaque deposition (11C-Pittsburgh compound B), a

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Kambe, Taiki, Yumiko Motoi, Kenji Ishii, and Nobutaka Hattori. "Posterior cortical atrophy with [11C] Pittsburgh compound B accumulation in the primary visual cortex." Journal of Neurology 257, no. 3 (2009): 469–71. http://dx.doi.org/10.1007/s00415-009-5377-y.

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5

Vlassenko, Andrei G., Mark A. Mintun, Chengjie Xiong, et al. "Amyloid-beta plaque growth in cognitively normal adults: Longitudinal [11C]Pittsburgh compound B data." Annals of Neurology 70, no. 5 (2011): 857–61. http://dx.doi.org/10.1002/ana.22608.

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Grimmer, Timo, Panagiotis Alexopoulos, Amalia Tsolakidou, et al. "Cerebrospinal Fluid BACE1 Activity and Brain Amyloid Load in Alzheimer's Disease." Scientific World Journal 2012 (2012): 1–6. http://dx.doi.org/10.1100/2012/712048.

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The secretase BACE1 is fundamentally involved in the development of cerebral amyloid pathology in Alzheimer's disease (AD). It has not been studied so far to what extent BACE1 activity in cerebrospinal fluid (CSF) mirrors in vivo amyloid load in AD. We explored associations between CSF BACE1 activity and fibrillar amyloid pathology as measured by carbon-11-labelled Pittsburgh Compound B positron emission tomography ([11C]PIB PET). [11C]PIB and CSF studies were performed in 31 patients with AD. Voxel-based linear regression analysis revealed significant associations between CSF BACE1 activity a

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Cai, Han, Su Ning, Wei Li, Xia Li, Shifu Xiao, and Lin Sun. "Patient with frontal-variant syndrome in early-onset Alzheimer's disease." General Psychiatry 33, no. 2 (2020): e100173. http://dx.doi.org/10.1136/gpsych-2019-100173.

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The clinical manifestation of frontal-variant Alzheimer’s disease (fvAD) is not typical, and it is difficult yet necessary to differentiate fvAD from frontal-variant frontal temporal dementia (fvFTD). We describe a patient with early-onset Alzheimer’s disease (AD) who presented with an fvFTD-like syndrome and apolipoprotein E ɛ3/ ɛ4 genotype. A brain amyloid imaging procedure, 11C-Pittsburgh compound B positron emission tomography (PET), supported the final diagnosis of AD. Our present case highlights the clinical variability that characterises early-onset AD. A multimodal approach is crucial

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Zwan, M. D., R. Ossenkoppele, N. Tolboom, et al. "Comparison of Simplified Parametric Methods for Visual Interpretation of 11C-Pittsburgh Compound-B PET Images." Journal of Nuclear Medicine 55, no. 8 (2014): 1305–7. http://dx.doi.org/10.2967/jnumed.114.139121.

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Sato, Koichi, Kiyoshi Fukushi, Hitoshi Shinotoh, et al. "Noninvasive k3 estimation method for slow dissociation PET ligands: application to [11C]Pittsburgh compound B." EJNMMI Research 3, no. 1 (2013): 76. http://dx.doi.org/10.1186/2191-219x-3-76.

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10

Ikoma, Yoko, Paul Edison, Anil Ramlackhansingh, David J. Brooks, and Federico E. Turkheimer. "Reference Region Automatic Extraction in Dynamic [11C]PIB." Journal of Cerebral Blood Flow & Metabolism 33, no. 11 (2013): 1725–31. http://dx.doi.org/10.1038/jcbfm.2013.133.

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The positron emission tomography (PET) radiotracer [11C]Pittsburgh Compound B (PIB) is a marker of amyloid plaque deposition in brain, and binding potential is usually quantified using the cerebellum as a reference where the specific binding is negligible. The use of the cerebellum as a reference, however, has been questioned by the reported cerebellar [11C]PIB retention in familial Alzheimer's disease (AD) subjects. In this work, we developed a supervised clustering procedure for the automatic extraction of a reference region in [11C]PIB studies. Supervised clustering models each gray matter

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11

Toppala, Sini, Laura L. Ekblad, Jouni Tuisku та ін. "Association of Early β-Amyloid Accumulation and Neuroinflammation Measured With [11C]PBR28 in Elderly Individuals Without Dementia". Neurology 96, № 12 (2021): e1608-e1619. http://dx.doi.org/10.1212/wnl.0000000000011612.

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ObjectiveTo examine whether early β–amyloid (Aβ) accumulation and metabolic risk factors are associated with neuroinflammation in elderly individuals without dementia.MethodsWe examined 54 volunteers (mean age 70.0 years, 56% women, 51% APOE ɛ4 carriers) with the translocator protein (TSPO) tracer [11C]PBR28 to assess neuroinflammation and with [11C] Pittsburgh compound B (PiB) to assess cerebral Aβ accumulation. [11C]PBR28 and [11C]PiB standardized uptake value ratios (SUVRs) were quantified in 6 regions of interests by using the cerebellar cortex as a pseudo-reference and reference region, r

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Rodriguez-Vieitez, E., S. F. Carter, K. Chiotis, et al. "Comparison of Early-Phase 11C-Deuterium-L-Deprenyl and 11C-Pittsburgh Compound B PET for Assessing Brain Perfusion in Alzheimer Disease." Journal of Nuclear Medicine 57, no. 7 (2016): 1071–77. http://dx.doi.org/10.2967/jnumed.115.168732.

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13

Hashimoto, Tetsuya, Chiaki Yokota, Kazuhiro Koshino, et al. "Binding of 11C-Pittsburgh compound-B correlated with white matter injury in hypertensive small vessel disease." Annals of Nuclear Medicine 31, no. 3 (2017): 227–34. http://dx.doi.org/10.1007/s12149-017-1152-9.

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Adamczuk, Katarzyna, Jolien Schaeverbeke, Natalie Nelissen, et al. "Amyloid imaging in cognitively normal older adults: comparison between 18F-flutemetamol and 11C-Pittsburgh compound B." European Journal of Nuclear Medicine and Molecular Imaging 43, no. 1 (2015): 142–51. http://dx.doi.org/10.1007/s00259-015-3156-9.

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15

Shirvan, Julia, Nathan Clement, Rong Ye, et al. "Neuropathologic correlates of amyloid and dopamine transporter imaging in Lewy body disease." Neurology 93, no. 5 (2019): e476-e484. http://dx.doi.org/10.1212/wnl.0000000000007855.

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ObjectiveTo develop imaging biomarkers of diseases in the Lewy body spectrum and to validate these markers against postmortem neuropathologic findings.MethodsFour cognitively normal participants with Parkinson disease (PD), 4 with PD with cognitive impairments, and 10 with dementia with Lewy bodies underwent amyloid imaging with [11C]Pittsburgh compound B (PiB) and dopamine transporter (DAT) imaging with [11C]Altropane. All 18 had annual neurologic examinations. All cognitively normal participants with PD developed cognitive impairment before death. Neuropathologic examinations assessed and sc

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Okazawa, Hidehiko, Masamichi Ikawa, Tetsuya Tsujikawa, et al. "Noninvasive Measurement of [11C]PiB Distribution Volume Using Integrated PET/MRI." Diagnostics 10, no. 12 (2020): 993. http://dx.doi.org/10.3390/diagnostics10120993.

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A noninvasive image-derived input function (IDIF) method using PET/MRI was applied to quantitative measurements of [11C] Pittsburgh compound-B (PiB) distribution volume (DV) and compared with other metrics. Fifty-three patients suspected of early dementia (71 ± 11 y) underwent 70 min [11C]PiB PET/MRI. Nineteen of them (68 ± 11 y) without head motion during the scan were enrolled in this study and compared with 16 age-matched healthy controls (CTL: 68 ± 11 y). The dynamic frames reconstructed from listmode PET data were used for DV calculation. IDIF with metabolite correction was applied to the

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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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18

Farid, Karim, Stephen F. Carter, Elena Rodriguez-Vieitez, et al. "Case Report of Complex Amyotrophic Lateral Sclerosis with Cognitive Impairment and Cortical Amyloid Deposition." Journal of Alzheimer's Disease 47, no. 3 (2015): 661–67. https://doi.org/10.3233/JAD-141965.

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Amyotrophic lateral sclerosis (ALS), a fatal disease of unknown origin, affects motor neurons in the primary motor cortex, brainstem, and spinal cord. Cognitive impairment may occur before the motor symptoms. We present a patient who was initially diagnosed with mild cognitive impairment (MCI) due to Alzheimer’s disease (AD) but who developed ALS-like symptoms during follow-up and died shortly thereafter. A 60-year-old subject with cognitive impairment underwent neuropsychological testing, cerebrospinal fluid (CSF) analysis, structural imaging (computed tomography and magnetic resonance

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Shinotoh, Hitoshi, Hitoshi Shimada, Yasumasa Kokubo, et al. "Tau imaging detects distinctive distribution of tau pathology in ALS/PDC on the Kii Peninsula." Neurology 92, no. 2 (2018): e136-e147. http://dx.doi.org/10.1212/wnl.0000000000006736.

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ObjectiveTo characterize the distribution of tau pathology in patients with amyotrophic lateral sclerosis/parkinsonism dementia complex on the Kii Peninsula (Kii ALS/PDC) by tau PET using [11C]PBB3 as ligand.MethodsThis is a cross-sectional study of 5 patients with ALS/PDC and one asymptomatic participant with a dense family history of ALS/PDC from the Kii Peninsula who took part in this study. All were men, and their age was 76 ± 8 (mean ± SD) years. Thirteen healthy men (69 ± 6 years) participated as healthy controls (HCs). Dynamic PET scans were performed following injection of [11C]PBB3, a

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Gómez-Vallejo, Vanessa, and Jordi Llop. "Fully automated and reproducible radiosynthesis of high specific activity [11C]raclopride and [11C]Pittsburgh compound-B using the combination of two commercial synthesizers." Nuclear Medicine Communications 32, no. 11 (2011): 1011–17. http://dx.doi.org/10.1097/mnm.0b013e32834b45a3.

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21

Gao, Zhong-Bao, Wei Wang, Xing-Li Zhao, et al. "Multi-modality molecular imaging characteristics of dementia with Lewy bodies." Journal of International Medical Research 46, no. 6 (2018): 2317–26. http://dx.doi.org/10.1177/0300060518764749.

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Objective Dementia with Lewy bodies (DLB) is a common type of neurodegenerative dementia. Molecular neuroimaging using dopamine transporter (DaT), Pittsburgh compound B (PIB), and fluorodeoxyglucose (FDG) positron emission tomography (PET) has advantages in detecting dopaminergic neuron loss, abnormal amyloid β-protein deposition, and glucose metabolism changes in patients with neurodegenerative disorders. However, the multi-modality molecular imaging features of patients with DLB have rarely been reported. Methods Five patients with a probable diagnosis of DLB were enrolled. PET/magnetic reso

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Vanhaute, Heleen, Jenny Ceccarini, Laura Michiels, et al. "In vivo synaptic density loss is related to tau deposition in amnestic mild cognitive impairment." Neurology 95, no. 5 (2020): e545-e553. http://dx.doi.org/10.1212/wnl.0000000000009818.

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ObjectiveTo investigate in vivo whether synaptic loss and neurofibrillary tangle load spatially overlap and correlate with clinical symptoms in patients with amnestic mild cognitive impairment (aMCI).MethodsIn this cross-sectional study, 10 patients with aMCI and 10 healthy controls underwent triple PET-MRI with 11C-UCB-J (synaptic vesicle protein 2A), 18F-MK-6240 (tau deposition), and 11C-Pittsburgh compound B (β-amyloid) and neuropsychological assessment. Gray matter atrophy was assessed by voxel-based morphometry with T1-weighted MRIs. Voxel-wise and volume-of-interest analyses were conduct

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Leuzy, Antoine, Stephen F. Carter, Konstantinos Chiotis, Ove Almkvist, Anders Wall, and Agneta Nordberg. "Concordance and Diagnostic Accuracy of [11C]PIB PET and Cerebrospinal Fluid Biomarkers in a Sample of Patients with Mild Cognitive Impairment and Alzheimer's Disease." Journal of Alzheimer's Disease 45, no. 4 (2015): 1077–88. https://doi.org/10.3233/JAD-142952.

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Background: Alzheimer's disease (AD) pathology can be quantified in vivo using cerebrospinal fluid (CSF) levels of amyloid-β1-42 (Aβ1-42), total-tau (t-tau), and phosphorylated tau (p-tau181p), as well as with positron emission tomography (PET) using [11C]Pittsburgh compound-B ([11C]PIB). Studies assessing concordance between these measures, however, have provided conflicting results. Moreover, it has been proposed that [11C]PIB PET may be of great clinical utility in terms of identifying patients with mild cognitive impairment (MCI) who will progress to the dementia phase of AD.

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Kimura, Noriyuki, Miki Aikawa, Kasumi Etou, Yasuhiro Aso, and Etsuro Matsubara. "Association between Matrix Metalloproteinases, Their Tissue Inhibitor and White Matter Lesions in Mild Cognitive Impairment." Current Alzheimer Research 17, no. 6 (2020): 547–55. http://dx.doi.org/10.2174/1567205017666200810171322.

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Background: White matter lesions are frequently found in mild cognitive impairments and Alzheimer’s disease. Matrix metalloproteinases and the tissue inhibitor of metalloproteinases are implicated in amyloid-β catabolism and blood brain barrier permeability. However, it remains unclear whether they are associated with white matter lesions in Alzheimer’s disease. Objective: The aim of this study was to examine the association of matrix metalloproteinases and tissue inhibitor of metalloproteinases with white matter degeneration in subjects with amyloid-positive mild cognitive impairment. Methods

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Képes, Zita, Alexandra Barkóczi, Judit P. Szabó та ін. "In Vivo Preclinical Assessment of β-Amyloid–Affine [11C]C-PIB Accumulation in Aluminium-Induced Alzheimer’s Disease-Resembling Hypercholesterinaemic Rat Model". International Journal of Molecular Sciences 23, № 22 (2022): 13950. http://dx.doi.org/10.3390/ijms232213950.

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Aluminum (Al) excess and hypercholesterinaemia are established risks of Alzheimer’s disease (AD). The aim of this study was to establish an AD-resembling hypercholesterinaemic animal model—with the involvement of 8 week and 48 week-old Fischer-344 rats—by Al administration for the safe and rapid verification of β-amyloid-targeted positron emission tomography (PET) radiopharmaceuticals. Measurement of lipid parameters and β-amyloid–affine [11C]C-Pittsburgh Compound B ([11C]C-PIB) PET examinations were performed. Compared with the control, the significantly elevated cholesterol and LDL levels of

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Carter, S. F., M. Scholl, O. Almkvist, et al. "Evidence for Astrocytosis in Prodromal Alzheimer Disease Provided by 11C-Deuterium-L-Deprenyl: A Multitracer PET Paradigm Combining 11C-Pittsburgh Compound B and 18F-FDG." Journal of Nuclear Medicine 53, no. 1 (2012): 37–46. http://dx.doi.org/10.2967/jnumed.110.087031.

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Shu, Xinghui, Jiehui Jiang, Yu Song, Zhemin Huang, Yihui Guan, and Zhuangzhi Yan. "Incorporating Priori Structure Knowledge in Level Set Method-Based Algorithm for 11C-Pittsburgh Compound B Positron Emission Tomography Segmentation." Journal of Medical Imaging and Health Informatics 6, no. 4 (2016): 968–77. http://dx.doi.org/10.1166/jmihi.2016.1778.

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Chae, Sun Young, Hye Ok Kim, Minyoung Oh, et al. "Evaluation of Selective Positron Emission Tomography Template Method for Spatial Normalization of Amyloid Imaging With 11C-Pittsburgh Compound B." Journal of Computer Assisted Tomography 38, no. 6 (2014): 924–29. http://dx.doi.org/10.1097/rct.0000000000000123.

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Takasone, Ken, Nagaaki Katoh, Yusuke Takahashi, et al. "Non-invasive detection and differentiation of cardiac amyloidosis using 99mTc-pyrophosphate scintigraphy and 11C-Pittsburgh compound B PET imaging." Amyloid 27, no. 4 (2020): 266–74. http://dx.doi.org/10.1080/13506129.2020.1798223.

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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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Baron, Jean-Claude, Karim Farid, Eamon Dolan, et al. "Diagnostic Utility of Amyloid PET in Cerebral Amyloid Angiopathy-Related Symptomatic Intracerebral Hemorrhage." Journal of Cerebral Blood Flow & Metabolism 34, no. 5 (2014): 753–58. http://dx.doi.org/10.1038/jcbfm.2014.43.

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By detecting β-amyloid ( Aβ) in the wall of cortical arterioles, amyloid positron emission tomography (PET) imaging might help diagnose cerebral amyloid angiopathy (CAA) in patients with lobar intracerebral hemorrhage (I-ICH). No previous study has directly assessed the diagnostic value of 11-Pittsburgh compound B (PiB) PET in probable CAA-related I-ICH against healthy controls (HCs). 11C-PiB-PET and magnetic resonance imaging (MRI) including T2* were obtained in 11 nondemented patients fulfilling the Boston criteria for probable CAA-related symptomatic I-ICH (sl-ICH) and 20 HCs without cognit

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

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

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Hosokawa, C., K. Ishii, Y. Kimura, et al. "Performance of 11C-Pittsburgh Compound B PET Binding Potential Images in the Detection of Amyloid Deposits on Equivocal Static Images." Journal of Nuclear Medicine 56, no. 12 (2015): 1910–15. http://dx.doi.org/10.2967/jnumed.115.156414.

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Lowe, Val J., Emily S. Lundt, Matthew L. Senjem та ін. "White Matter Reference Region in PET Studies of 11C-Pittsburgh Compound B Uptake: Effects of Age and Amyloid-β Deposition". Journal of Nuclear Medicine 59, № 10 (2018): 1583–89. http://dx.doi.org/10.2967/jnumed.117.204271.

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Faria, Daniele de P., Fabio L. Duran, Paula Squarzoni, et al. "Topography of 11C-Pittsburgh compound B uptake in Alzheimer’s disease: a voxel-based investigation of cortical and white matter regions." Brazilian Journal of Psychiatry 41, no. 2 (2019): 101–11. http://dx.doi.org/10.1590/1516-4446-2017-0002.

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Abe, Y., N. Kimura, R. Takahashi, M. Goto, and E. Matsubara. "Relationship between cytokine levels in the cerebrospinal fluid and 11C-pittsburgh compound B retention in patients with mild cognitive impairment." Journal of the Neurological Sciences 381 (October 2017): 312. http://dx.doi.org/10.1016/j.jns.2017.08.885.

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Abe, Yoshitake, Noriyuki Kimura, Ryuichi Takahashi, et al. "Relationship between cytokine levels in the cerebrospinal fluid and 11C-Pittsburgh compound B retention in patients with mild cognitive impairment." Geriatrics & Gerontology International 17, no. 11 (2017): 1907–13. http://dx.doi.org/10.1111/ggi.12991.

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Kitamura, Soichiro, Hitoshi Shimada, Fumitoshi Niwa, et al. "Tau-induced focal neurotoxicity and network disruption related to apathy in Alzheimer’s disease." Journal of Neurology, Neurosurgery & Psychiatry 89, no. 11 (2018): 1208–14. http://dx.doi.org/10.1136/jnnp-2018-317970.

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ObjectiveApathy is a common neuropsychological symptom in Alzheimer’s disease (AD), and previous studies demonstrated that neuronal loss and network disruption in some brain regions play pivotal roles in the pathogenesis of apathy. However, contributions of tau and amyloid-β (Aβ) depositions, pathological hallmarks of AD, to the manifestation of apathy remain elusive.MethodsSeventeen patients with AD underwent positron emission tomography (PET) with11C-pyridinyl-butadienyl-benzothiazole 3 (11C-PBB3) and11C-Pittsburgh compound-B (11C-PiB) to estimate tau and Aβ accumulations using standardised

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Herholz, Karl. "Molecular Imaging in Alzheimer’s Disease." US Neurology 06, no. 02 (2010): 28. http://dx.doi.org/10.17925/usn.2010.06.02.28.

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The most sensitive and accurate method for molecular imaging in human Alzheimer’s disease (AD) is positron emission tomography (PET). The most widely available PET tracer, which is also used in clinical oncology, is 18F-2-fluoro-2-deoxy-D-glucose (FDG). FDG is an imaging biomarker for early and differential diagnosis of AD. Even higher molecular specificity and sensitivity for detection of AD before dementia onset is provided by high-affinity ligands for fibrillary amyloid. 11C-Pittsburgh Compound B is widely being used in research laboratories, while new 18F-labeled ligands are currently unde

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Liu, Fangyu, Ryan Dougherty, Amal Wanigatunga, et al. "Associations Between Perceived Fatigability and Amyloid Status in the Baltimore Longitudinal Study of Aging." Innovation in Aging 5, Supplement_1 (2021): 207. http://dx.doi.org/10.1093/geroni/igab046.799.

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Abstract Higher level of and greater longitudinal increase in perceived fatigability are linked to cognitive decline and lower brain volumes in older adults. However, it remains unclear whether perceived fatigability is associated with Alzheimer’s disease-related brain pathology. In the BLSA, 163 participants without neurological disease or cognitive impairment (aged 74.7+/-8.4 years, 45% men) were assessed for perceived fatigability using rating of perceived exertion after a 5-minute (0.67 m/s) treadmill walk and Aß burden using 11C-Pittsburgh compound B (PiB) positron emission tomography. Fo

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Dougherty, Ryan, Fangyu Li, Amal Wanigatunga, et al. "Association of Walking Energetics With Amyloid Status: Findings From the Baltimore Longitudinal Study of Aging." Innovation in Aging 5, Supplement_1 (2021): 369. http://dx.doi.org/10.1093/geroni/igab046.1433.

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Abstract Higher energetic costs for mobility are associated with slow and declining gait speed. Slow gait is linked to cognitive decline and Alzheimer’s disease (AD), but the physiological underpinnings are note well-understood. We investigated the cross-sectional association between the energetic cost of walking and amyloid status (+/-) in 174 cognitively unimpaired men and women (52%) aged 78.5±8.6 years. The energetic cost of walking was assessed as the average oxygen consumption (VO2) during 2.5 minutes of customary-paced overground walking. Amyloid status was determined from 11C-Pittsburg

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Kehrer-Dunlap, Abigail, Rebecca Bollinger, Szu-Wei Chen, et al. "Higher amyloid correlates to greater loneliness during the COVID-19 pandemic." F1000Research 11 (October 4, 2022): 1134. http://dx.doi.org/10.12688/f1000research.124891.1.

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Background: Little is known about psychosocial characteristics, including loneliness, anxiety, and depression, present in preclinical Alzheimer disease (AD). The purpose of this cross-sectional study was to examine the relationship between these psychosocial characteristics and amyloid accumulation in cognitively normal older adults with and without preclinical AD during the COVID-19 pandemic. Methods: A global Clinical Dementia Rating® Scale score of 0 was required for enrollment. Cortical amyloid burden was measured using [11C] Pittsburgh compound B or [18F]-Florbetapir PET tracers. Centiloi

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Couto, Paul J., and Richard M. Millis. "PET Imaging of Epigenetic Influences on Alzheimer’s Disease." International Journal of Alzheimer's Disease 2015 (2015): 1–11. http://dx.doi.org/10.1155/2015/575078.

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The precise role of environment-gene interactions (epigenetics) in the development and progression of Alzheimer’s disease (AD) is unclear. This review focuses on the premise that radiotracer-specific PET imaging allows clinicians to visualize epigenetically influenced events and that such imaging may provide new, valuable insights for preventing, diagnosing, and treating AD. Current understanding of the role of epigenetics in AD and the principles underlying the use of PET radiotracers forin vivodiagnosis are reviewed. The relative efficacies of various PET radiotracers for visualizing the epi

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Herholz, Karl. "Molecular Imaging in Alzheimer’s Disease." European Neurological Review 6, no. 1 (2011): 16. http://dx.doi.org/10.17925/enr.2011.06.01.16.

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The most sensitive and accurate method for molecular imaging in human Alzheimer’s disease (AD) is positron emission tomography (PET). The most widely available PET tracer, which is also used in clinical oncology, is 18F-2-fluoro-2-deoxy-D-glucose (FDG). FDG is an imaging biomarker for early and differential diagnosis of AD. Even higher molecular specificity and sensitivity for detection of AD before dementia onset is provided by high-affinity ligands for fibrillary amyloid. 11C-Pittsburgh Compound B is widely being used in research laboratories, while new 18F-labelled ligands are currently und

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Grimmer, Timo, Oliver Goldhardt, Igor Yakushev, et al. "Associations of Neprilysin Activity in CSF with Biomarkers for Alzheimer’s Disease." Neurodegenerative Diseases 19, no. 1 (2019): 43–50. http://dx.doi.org/10.1159/000500811.

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Background: Neprilysin (NEP) cleaves amyloid-β 1–42 (Aβ42) in the brain. Hence, we aimed to elucidate the effect of NEP on Aβ42 in cerebrospinal fluid (CSF) and on in vivo brain amyloid load using amyloid positron emission tomography (PET) with [11C]PiB (Pittsburgh compound B). In addition, associations with the biomarkers for neuronal injury, CSF-tau and FDG-PET, were investigated. Methods: Associations were calculated using global and voxel-based (SPM8) linear regression analyses in the same cohort of 23 highly characterized Alzheimer’s disease patients. Results: CSF-NEP was significantly in

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Shi, Zhihong, Ying Wang, Shuai Liu, et al. "Clinical and Neuroimaging Characterization of Chinese Dementia Patients with PSEN1 and PSEN2 Mutations." Dementia and Geriatric Cognitive Disorders 39, no. 1-2 (2014): 32–40. http://dx.doi.org/10.1159/000366272.

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Background: Alzheimer's disease (AD) and frontotemporal dementia (FTD) are two common forms of primary neurodegenerative dementia. Mutations in 3 genes (PSEN1, PSEN2, and APP) have been identified in patients with early-onset AD. Methods: We performed gene sequencing in PSEN1, PSEN2, and APP in 61 AD and 35 FTD Chinese patients. Amyloid load using 11C-labeled Pittsburgh compound B (11C-PIB) positron emission tomography (PET) and cerebral glucose metabolism using 18F-fludeoxyglucose PET were evaluated in patients carrying mutations. Results: We identified 1 known pathogenic PSEN1 (p.His163Arg,

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Meyer, P. T., S. Hellwig, F. Amtage, et al. "Dual-Biomarker Imaging of Regional Cerebral Amyloid Load and Neuronal Activity in Dementia with PET and 11C-Labeled Pittsburgh Compound B." Journal of Nuclear Medicine 52, no. 3 (2011): 393–400. http://dx.doi.org/10.2967/jnumed.110.083683.

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Zhou, Yun, Susan M. Resnick, Weiguo Ye, et al. "Using a reference tissue model with spatial constraint to quantify [11C]Pittsburgh compound B PET for early diagnosis of Alzheimer's disease." NeuroImage 36, no. 2 (2007): 298–312. http://dx.doi.org/10.1016/j.neuroimage.2007.03.004.

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Zhou, Zhi, Martijn L. T. M. Müller, Prabesh Kanel та ін. "Apathy rating scores and β-amyloidopathy in patients with Parkinson disease at risk for cognitive decline". Neurology 94, № 4 (2019): e376-e383. http://dx.doi.org/10.1212/wnl.0000000000008683.

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ObjectiveTo determine whether β-amyloidopathy correlates with apathy rating scores independently of mood changes and other neurodegenerative processes in Parkinson disease (PD).MethodsIn this cross-sectional study, patients with PD (n = 64, 48 male and 16 female, mean age 69.2 ± 6.7 years, Hoehn & Yahr stage 2.7 ± 0.5, Montreal Cognitive Assessment score 25.3 ± 3.0) underwent [11C]Pittsburgh compound B β-amyloid, [11C]dihydrotetrabenazine vesicular monoamine transporter type 2 (VMAT2), and [11C]methyl 4 piperidinyl propionate acetylcholinesterase brain PET imaging and clinical assessments,

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