ArticleAmerican journal of nuclear medicine and molecular imaging2016
[(11)C]PiB PET in Gerstmann-Sträussler-Scheinker disease.
Article in American journal of nuclear medicine and molecular imaging, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.
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.
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Who cites it
8 citing papers in PubMed, 1 synthesis or guideline pooled it, 9 citations in OpenAlex.
- Genome-wide association study of brain amyloid deposition as measured by Pittsburgh Compound-B (PiB)-PET imaging.Molecular psychiatry · 2021Pooled it
- Distinctive properties of the prion protein in the brain and retina in the amyloidosis associated with the PRNP F198S mutation.Acta neuropathologica · 2026Article
- Distinctive properties of the prion protein in the brain and retina in the amyloidosis associated with the PRNP F198S Mutation.Research square · 2026Article
- Parkinsonism in Gerstmann-Sträussler-Scheinker disease: A case report.eNeurologicalSci · 2025Article
- Biological Fluid Biomarkers in Human Prion Diseases with a Note on Biosafety.Sub-cellular biochemistry · 2025Review
- The Role of PET Imaging in Patients with Prion Disease: A Literature Review.Molecular imaging and biology · 2024Review
- Detection of tau in Gerstmann-Sträussler-Scheinker disease (PRNP F198S) by [Acta neuropathologica communications · 2018Article
- Cognitive Decline: Not Always Alzheimer's Disease.Journal of Alzheimer's disease reports · 2018Article
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
Gerstmann-Sträussler-Scheinker Disease (GSS) is a familial neurodegenerative disorder characterized clinically by ataxia, parkinsonism, and dementia, and neuropathologically by deposition of diffuse and amyloid plaques composed of prion protein (PrP). The purpose of this study was to evaluate if [(11)C]Pittsburgh Compound B (PiB) positron emission tomography (PET) is capable of detecting PrP-amyloid in PRNP gene carriers. Six individuals at risk for GSS and eight controls underwent [(11)C]PiB PET scans using standard methods. Approximately one year after the initial scan, each of the three asymptomatic carriers (two with PRNP P102L mutation, one with PRNP F198S mutation) underwent a second [(11)C]PiB PET scan. Three P102L carriers, one F198S carrier, and one non-carrier of the F198S mutation were cognitively normal, while one F198S carrier was cognitively impaired during the course of this study. No [(11)C]PiB uptake was observed in any subject at baseline or at follow-up. Neuropathologic study of the symptomatic individual revealed PrP-immunopositive plaques and tau-immunopositive neurofibrillary tangles in cerebral cortex, subcortical nuclei, and brainstem. PrP deposits were also numerous in the cerebellar cortex. This is the first study to investigate the ability of [(11)C]PiB PET to bind to PrP-amyloid in GSS F198S subjects. This finding suggests that [(11)C]PiB PET is not suitable for in vivo assessment of PrP-amyloid plaques in patients with GSS.
Indexed as
Identifiers
27069768PMC4749507W2338727013What OpenQuestion holds
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.