Relevant bibliographies by topics / 11C-Pittsburgh compound B

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  1. Journal articles
  2. Dissertations / Theses
  3. Book chapters
  4. Conference papers

Academic literature on the topic '11C-Pittsburgh compound B'

Author: Grafiati
Published: 2 June 2025
Last updated: 31 July 2025

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

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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-&beta; deposition in the human brain&nbsp;<em>in vivo</em>&nbsp;by positron emission tomography has improved our understanding of the time course of amyloid-&beta; pathology in Alzheimer&rsquo;s disease. The most widely used amyloid-&beta; imaging tracer so far is&nbsp;11C-Pittsburgh compound B, a thioflavin derivative but other&nbsp;11C- and&nbsp;18F-labelled amyloid-&beta; tracers have been studied in patients with Alzheimer&#39;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&rsquo;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&rsquo;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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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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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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Dissertations / Theses on the topic "11C-Pittsburgh compound B"

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Pais, Marta Silva Lapo. "Machine Learning Classification in Alzheimer’s disease based on 11C-Pittsburgh Compound B (PiB) and 11C-(R)-PK11195 (PK) PET imaging measures and the correlation between these two biomarkers." Master's thesis, 2019. http://hdl.handle.net/10316/87968.

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Trabalho de Projeto do Mestrado Integrado em Engenharia Biomédica apresentado à Faculdade de Ciências e Tecnologia<br>A doença de Alzheimer (AD) é a doença neurodegenerativa responsável pelo maior número de casos de demência. Tomografia por emissão de positrões (PET) com 11C-Pittsburgh Compound B (PiB) e 11C-(R)-PK11195 (PK) são duas modalidades utilizadas na visualização das placas amilóides e da microglia ativada no cérebro humano, respetivamente. Uma vez que as placas amilóides são o principal identificador da AD e que a microglia ativada é também recorrentemente encontrada no cérebro dos
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Book chapters on the topic "11C-Pittsburgh compound B"

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Høilund-Carlsen, Poul F., Abass Alavi, and Jorge R. Barrio. "PET/CT/MRI in Clinical Trials of Alzheimer’s Disease." In Advances in Alzheimer’s Disease. IOS Press, 2024. https://doi.org/10.3233/aiad240044.

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With the advent of PET imaging in 1976, 2-deoxy-2-[18F]fluoro-D-glucose (FDG)-PET became the preferred method for in vivo investigation of cerebral processes, including regional hypometabolism in Alzheimer’s disease. With the emergence of amyloid-PET tracers, [11C]Pittsburgh Compound-B in 2004 and later [18F]florbetapir, [18F]florbetaben, and [18F]flumetamol, amyloid-PET has replaced FDG-PET in Alzheimer’s disease anti-amyloid clinical trial treatments to ensure “amyloid positivity” as an entry criterion, and to measure treatment-related decline in cerebral amyloid deposits. MRI has been used
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Conference papers on the topic "11C-Pittsburgh compound B"

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Parmera, Jacy, Artur Coutinho, Isabel Almeida, et al. "CORTICOBASAL SYNDROME: A PROSPECTIVE STUDY OF CLINICAL PROFILES AND IMAGING BIOMARKERS." In XIII Meeting of Researchers on Alzheimer's Disease and Related Disorders. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1980-5764.rpda010.

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Background: Corticobasal syndrome (CBS) is neurodegenerative disorder related to multiple underlying pathologies. Objective: To investigated if dividual FDG-PET patterns could distinguish CBS due to Alzheimer’s disease (AD) from other pathologies based on [11C]Pittsburgh Compound-B (PIB)-PET. Methods: Forty-five patients with probable CBS were prospectively evaluated. They underwent FDG-PET and were divided into groups: related to AD (CBS FDG-AD) or non-AD (CBS FDG-nonAD). Thirty patients underwent PIB-PET on a PET-MRI to assess their amyloid status. FDG and PIB-PET were classified individuall
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Journal articles
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