ArticleBrain : a journal of neurology2007
Thalamic metabolism and symptom onset in preclinical Huntington's disease.
Article in Brain : a journal of neurology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers, 2 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
95 citing papers in PubMed, 2 syntheses or guidelines pooled it, 196 citations in OpenAlex.
- The Role of the Cerebellum in Huntington's Disease: a Systematic Review.Cerebellum (London, England) · 2021Pooled it
- Current status of PET imaging in Huntington's disease.European journal of nuclear medicine and molecular imaging · 2016Pooled it
- Pepinemab antibody blockade of SEMA4D in early Huntington's disease: a randomized, placebo-controlled, phase 2 trial.Nature medicine · 2022Trial
- Spontaneous speech and language measures as predictive biomarkers of clinically meaningful disease progression and neurodegeneration in Huntington's disease.Journal of neural transmission (Vienna, Austria : 1996) · 2026Article
- Progressively reduced cerebral oxygen metabolism and elevated plasma NfL levels in the zQ175DN mouse model of Huntington's disease.Experimental neurology · 2025Article
- Development of cognitive, motor, metabolic, and mutant huntingtin aggregation in the zQ175 mouse model of Huntington's disease.Scientific reports · 2025Article
- Musical Distractions: Music-Based Rhythmic Auditory Stimulation Fails to Improve Gait in Huntington's Disease.Brain sciences · 2025Article
- Advances in Huntington's Disease Biomarkers: A 10-Year Bibliometric Analysis and a Comprehensive Review.Biology · 2025Review
- In defence of ferroptosis.Signal transduction and targeted therapy · 2025Review
- Pediatric Huntington Disease Brains Have Distinct Morphologic and Metabolic Traits: the RAREST-JHD Study.Movement disorders clinical practice · 2024Article
- Altered Iron and Microstructure in Huntington's Disease Subcortical Nuclei: Insight From 7T MRI.Journal of magnetic resonance imaging : JMRI · 2024Article
- Clinical Review of Juvenile Huntington's Disease.Journal of Huntington's disease · 2024Review
- Thalamic Foxp2 regulates output connectivity and sensory-motor impairments in a model of Huntington's Disease.Cellular and molecular life sciences : CMLS · 2023Article
- Integrated multi-omics analysis of Huntington disease identifies pathways that modulate protein aggregation.Disease models & mechanisms · 2022Article
- Spatial normalization and quantification approaches of PET imaging for neurological disorders.European journal of nuclear medicine and molecular imaging · 2022Review
- EANM procedure guidelines for brain PET imaging using [European journal of nuclear medicine and molecular imaging · 2022Article
- Huntingtin silencing delays onset and slows progression of Huntington's disease: a biomarker study.Brain : a journal of neurology · 2021Article
- Glucose metabolic crosstalk and regulation in brain function and diseases.Progress in neurobiology · 2021Review
- Hybrid 2-[18F] FDG PET/MRI in premanifest Huntington's disease gene-expansion carriers: The significance of partial volume correction.PloS one · 2021Article
- Endocannabinoids and Dopamine Balance Basal Ganglia Output.Frontiers in cellular neuroscience · 2021Article
35 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 5 institutions in 2 countries.
Funding
Abstract
The neural basis for the transition from preclinical to symptomatic Huntington's disease (HD) is unknown. We used serial positron emission tomography (PET) imaging in preclinical HD gene carriers (p-HD) to assess the metabolic changes that occur during this period. Twelve p-HD subjects were followed longitudinally with [11C]-raclopride and [18F]-fluorodeoxyglucose PET imaging, with scans at baseline, 18 and 44 months. Progressive declines in striatal D2-receptor binding were correlated with concurrent changes in regional metabolism and in the activity of an HD-related metabolic network. We found that striatal D2 binding declined over time (P < 0.005). The activity of a reproducible HD-related metabolic covariance pattern increased between baseline and 18 months (P < 0.003) but declined at 44 months (P < 0.04). These network changes coincided with progressive declines in striatal and thalamic metabolic activity (P < 0.01). Striatal metabolism was abnormally low at all time points (P < 0.005). By contrast, thalamic metabolism was elevated at baseline (P < 0.01), but fell to subnormal levels in the p-HD subjects who developed symptoms. These findings were confirmed with an MRI-based atrophy correction for each individual PET scan. Increases in network expression and thalamic glucose metabolism may be compensatory for early neuronal losses in p-HD. Declines in these measures may herald the onset of symptoms in gene carriers.
Indexed as
Identifiers
What 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.