ArticleEuropean journal of nuclear medicine and molecular imaging2012
18F-FDG PET uptake in the pre-Huntington disease caudate affects the time-to-onset independently of CAG expansion size.
Article in European journal of nuclear medicine and molecular imaging, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
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Who cites it
28 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Current status of PET imaging in Huntington's disease.European journal of nuclear medicine and molecular imaging · 2016Pooled it
- Downregulation of Pten Improves Huntington's Disease Phenotype by Reducing Htt Aggregates and Cell Death.Molecular neurobiology · 2025Article
- Neuroimaging to Facilitate Clinical Trials in Huntington's Disease: Current Opinion from the EHDN Imaging Working Group.Journal of Huntington's disease · 2024Review
- Potential disease-modifying therapies for Huntington's disease: lessons learned and future opportunities.The Lancet. Neurology · 2022Review
- EANM procedure guidelines for brain PET imaging using [European journal of nuclear medicine and molecular imaging · 2022Article
- Movement Disorder in Wilson Disease: Correlation with MRI and Biomarkers of Cell Injury.Journal of molecular neuroscience : MN · 2021Article
- Hybrid 2-[18F] FDG PET/MRI in premanifest Huntington's disease gene-expansion carriers: The significance of partial volume correction.PloS one · 2021Article
- Manganese Acts upon Insulin/IGF Receptors to Phosphorylate AKT and Increase Glucose Uptake in Huntington's Disease Cells.Molecular neurobiology · 2020Article
- Multiple clinical features of Huntington's disease correlate with mutant HTT gene CAG repeat lengths and neurodegeneration.Journal of neurology · 2019Review
- Novel Imaging Biomarkers for Huntington's Disease and Other Hereditary Choreas.Current neurology and neuroscience reports · 2018Review
- Clinical utility of FDG-PET in amyotrophic lateral sclerosis and Huntington's disease.European journal of nuclear medicine and molecular imaging · 2018Review
- Altered lactate metabolism in Huntington's disease is dependent on GLUT3 expression.CNS neuroscience & therapeutics · 2018Article
- Article
- Molecular Imaging Markers to Track Huntington's Disease Pathology.Frontiers in neurology · 2017Review
- Functional neuroimaging and chorea: a systematic review.Journal of clinical movement disorders · 2017Review
- Statistical modeling of Huntington disease onset.Handbook of clinical neurology · 2017Review
- How reliable isEuropean journal of nuclear medicine and molecular imaging · 2016Article
- Striatal hypometabolism in premanifest and manifest Huntington's disease patients.European journal of nuclear medicine and molecular imaging · 2016Article
- Adenosine A1 receptor antagonist rolofylline alleviates axonopathy caused by human Tau ΔK280.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- The phasor-FLIM fingerprints reveal shifts from OXPHOS to enhanced glycolysis in Huntington Disease.Scientific reports · 2016Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeTo test in a longitudinal follow-up study whether basal glucose metabolism in subjects with a genetic risk of Huntington disease (HD) may influence the onset of manifest symptoms.
methodsThe study group comprised 43 presymptomatic (preHD) subjects carrying the HD mutation. They underwent a (18)F-FDG PET scan and were prospectively followed-up for at least 5 years using the unified HD rating scale to detect clinical changes. Multiple regression analysis included subject's age, CAG mutation size and glucose uptake as variables in a model to predict age at onset.
resultsOf the 43 preHD subjects who manifested motor symptoms, suggestive of HD, after 5 years from the PET scan, 26 showed a mean brain glucose uptake below the cut-off of 1.0493 in the caudate, significantly lower than the 17 preHD subjects who remained symptom-free (P < 0.0001). This difference was independent of mutation size. Measurement of brain glucose uptake improved the CAG repeat number and age-based model for predicting age at onset by 37 %.
conclusionA reduced level of glucose metabolism in the brain caudate may represent a predisposing factor that contributes to the age at onset of HD in preHD subjects, in addition to the mutation size.
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Registered trials
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