Trial reportEuropean journal of nuclear medicine and molecular imaging2010
In vivo detection of prion amyloid plaques using [(11)C]BF-227 PET.
Trial report in European journal of nuclear medicine and molecular imaging, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 36 citations in OpenAlex.
- The Role of PET Imaging in Patients with Prion Disease: A Literature Review.Molecular imaging and biology · 2024Review
- Combined findings of FDG-PET and arterial spin labeling in sporadic Creutzfeldt-Jakob disease.Prion · 2018Article
- A Pyridazine-Based Fluorescent Probe Targeting AJournal of analytical methods in chemistry · 2018Article
- Article
- [(11)C]PiB PET in Gerstmann-Sträussler-Scheinker disease.American journal of nuclear medicine and molecular imaging · 2016Article
- Characterisation of radioiodinated flavonoid derivatives for SPECT imaging of cerebral prion deposits.Scientific reports · 2015Article
- A 18F-labeled BF-227 derivative as a potential radioligand for imaging dense amyloid plaques by positron emission tomography.Molecular imaging and biology · 2013Article
- Amyloid-β probes: Review of structure-activity and brain-kinetics relationships.Beilstein journal of organic chemistry · 2013Article
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeIn vivo detection of pathological prion protein (PrP) in the brain is potentially useful for the diagnosis of transmissible spongiform encephalopathies (TSEs). However, there are no non-invasive ante-mortem means for detection of pathological PrP deposition in the brain. The purpose of this study is to evaluate the amyloid imaging tracer BF-227 with positron emission tomography (PET) for the non-invasive detection of PrP amyloid in the brain.
methodsThe binding ability of BF-227 to PrP amyloid was investigated using autoradiography and fluorescence microscopy. Five patients with TSEs, including three patients with Gerstmann-Sträussler-Scheinker disease (GSS) and two patients with sporadic Creutzfeldt-Jakob disease (CJD), underwent [(11)C]BF-227 PET scans. Results were compared with data from 10 normal controls and 17 patients with Alzheimer's disease (AD). The regional to pons standardized uptake value ratio was calculated as an index of BF-227 retention.
resultsBinding of BF-227 to PrP plaques was confirmed using brain samples from autopsy-confirmed GSS cases. In clinical PET study, significantly higher retention of BF-227 was detected in the cerebellum, thalamus and lateral temporal cortex of GSS patients compared to that in the corresponding tissues of normal controls. GSS patients also showed higher retention of BF-227 in the cerebellum, thalamus and medial temporal cortex compared to AD patients. In contrast, the two CJD patients showed no obvious retention of BF-227 in the brain.
conclusionAlthough [(11)C]BF-227 is a non-specific imaging marker of cerebral amyloidosis, it is useful for in vivo detection of PrP plaques in the human brain in GSS, based on the regional distribution of the tracer. PET amyloid imaging might provide a means for both early diagnosis and non-invasive disease monitoring of certain forms of TSEs.
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