ArticleMolecular imaging and biology2015
Preclinical Comparison of the Amyloid-β Radioligands [(11)C]Pittsburgh compound B and [(18)F]florbetaben in Aged APPPS1-21 and BRI1-42 Mouse Models of Cerebral Amyloidosis.
Article in Molecular imaging and biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
5 citing papers in PubMed.
- PET Imaging in Animal Models of Alzheimer's Disease.Frontiers in neuroscience · 2022Review
- Comparison of the Amyloid Load in the Brains of Two Transgenic Alzheimer's Disease Mouse Models Quantified by Florbetaben Positron Emission Tomography.Frontiers in neuroscience · 2021Article
- Assessment of brain beta-amyloid deposition in transgenic mouse models of Alzheimer's disease with PET imaging agentsBMC neuroscience · 2018Article
- Longitudinal Characterization of [18F]-FDG and [18F]-AV45 Uptake in the Double Transgenic TASTPM Mouse Model.Journal of Alzheimer's disease : JAD · 2017Article
- In vivo molecular neuroimaging of glucose utilization and its association with fibrillar amyloid-β load in aged APPPS1-21 mice.Alzheimer's research & therapy · 2015Article
Corrections and comments
- Erratum issued
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeThe aim of this study was to compare [(11)C]Pittsburgh compound B ([(11)C]PiB) and [(18)F]florbetaben ([(18)F]FBB) for preclinical investigations of amyloid-β pathology. PROCEDURES: We investigated two aged animal models of cerebral amyloidosis with contrasting levels of amyloid-β relating to "high" (APPPS1-21 n = 6, wild type (WT) n = 7) and "low" (BRI1-42 n = 6, WT n = 6) target states, respectively.
resultsAPPPS1-21 mice (high target state) demonstrated extensive fibrillar amyloid-β deposition that translated to significantly increased retention of [(11)C]PiB and [(18)F]FBB in comparison to their wild type. The retention pattern of [(11)C]PiB and [(18)F]FBB in this cohort displayed a significant correlation. However, the relative difference in tracer uptake between diseased and healthy mice was substantially higher for [(11)C]PiB than for [(18)F]FBB. Although immunohistochemistry confirmed the high plaque load in APPPS1-21 mice, correlation between tracer uptake and ex vivo quantification of amyloid-β was poor for both tracers. BRI1-42 mice (low target state) did not demonstrate increased tracer uptake.
conclusionsIn cases of high fibrillar amyloid-β burden, both tracers detected significant differences between diseased and healthy mice, with [(11)C]PiB showing a larger dynamic range.
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Identifiers
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.