ArticleJournal of clinical neurology (Seoul, Korea)2013
Decreased Metabolism in the Cerebral Cortex in Early-Stage Huntington's Disease: A Possible Biomarker of Disease Progression?
Article in Journal of clinical neurology (Seoul, Korea), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
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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
21 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
- Neuroimaging to Facilitate Clinical Trials in Huntington's Disease: Current Opinion from the EHDN Imaging Working Group.Journal of Huntington's disease · 2024Review
- Recent Advances in the Roles of MicroRNA and MicroRNA-Based Diagnosis in Neurodegenerative Diseases.Biosensors · 2022Review
- Pathogenesis of Huntington's Disease: An Emphasis on Molecular Pathways and Prevention by Natural Remedies.Brain sciences · 2022Review
- Metabolism in Huntington's disease: a major contributor to pathology.Metabolic brain disease · 2022Review
- The Use, Standardization, and Interpretation of Brain Imaging Data in Clinical Trials of Neurodegenerative Disorders.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021Review
- 18F-FDG PET/CT: an unexpected case of Huntington's disease.BMC neurology · 2019Article
- Platelet-derived extracellular vesicles in Huntington's disease.Journal of neurology · 2018Article
- Translation of MicroRNA-Based Huntingtin-Lowering Therapies from Preclinical Studies to the Clinic.Molecular therapy : the journal of the American Society of Gene Therapy · 2018Review
- Molecular Imaging Markers to Track Huntington's Disease Pathology.Frontiers in neurology · 2017Review
- Striatal hypometabolism in premanifest and manifest Huntington's disease patients.European journal of nuclear medicine and molecular imaging · 2016Article
- The phasor-FLIM fingerprints reveal shifts from OXPHOS to enhanced glycolysis in Huntington Disease.Scientific reports · 2016Article
- PET Imaging in Huntington's Disease.Journal of Huntington's disease · 2015Review
- Enhanced neuronal glucose transporter expression reveals metabolic choice in a HD Drosophila model.PloS one · 2015Article
- Current Status of Huntington's Disease in Korea: A Nationwide Survey and National Registry Analysis.Journal of movement disorders · 2015Article
- Neuroimaging in Huntington's disease.World journal of radiology · 2014Review
- Copy-number variation of the neuronal glucose transporter gene SLC2A3 and age of onset in Huntington's disease.Human molecular genetics · 2014Article
- Genetics of Huntington disease.AJNR. American journal of neuroradiology · 2014Article
- Is synaptic loss a unique hallmark of Alzheimer's disease?Biochemical pharmacology · 2014Review
- Huntington disease: natural history, biomarkers and prospects for therapeutics.Nature reviews. Neurology · 2014Review
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeHuntington's disease (HD) is an autosomal-dominant inherited neurodegenerative disorder. Genetic analysis of abnormal CAG expansion in the IT15 gene allows disease confirmation even in the preclinical stage. However, because there is no treatment to cure or delay the progression of this disease, monitoring of biological markers that predict progression is warranted.
methodsFDG-PET was applied to 13 patients with genetically confirmed HD in the early stage of the disease. We recorded the initial and follow-up statuses of patients using the Independence Scale (IS) of the Unified Huntington's Disease Rating Scale. The progression rate (PR) was calculated as the annual change in the IS. The patients were divided into two groups with faster and slower progression, using the median value of the PR as the cut-off. FDG-PET data were analyzed using regions of interest, and compared among the two patient groups and 11 age- and sex-matched controls.
resultsThe mean CAG repeat size in patients was 44.7. The CAG repeat length was inversely correlated with the age at onset as reported previously, but was not correlated with the clinical PR. Compared with normal controls, hypometabolism was observed even at very early stages of the disease in the bilateral frontal, temporal, and parietal cortices on FDG-PET. The decreases in metabolism in the bilateral frontal, parietal, and right temporal cortices were much greater in the faster-progression group than in the slower-progression group.
conclusionsA decrease in cortical glucose metabolism is suggested as a predictor for identifying a more rapid form of progression in patients with early-stage HD.
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Registered trials
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