ArticleEuropean journal of nuclear medicine and molecular imaging2014
Cross sectional PET study of cerebral adenosine A₁ receptors in premanifest and manifest Huntington's disease.
Article in European journal of nuclear medicine and molecular imaging, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis 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
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.
- Current status of PET imaging in Huntington's disease.European journal of nuclear medicine and molecular imaging · 2016Pooled it
- Advances in Huntington's Disease Biomarkers: A 10-Year Bibliometric Analysis and a Comprehensive Review.Biology · 2025Review
- Pediatric Huntington Disease Brains Have Distinct Morphologic and Metabolic Traits: the RAREST-JHD Study.Movement disorders clinical practice · 2024Article
- Microglia and complement mediate early corticostriatal synapse loss and cognitive dysfunction in Huntington's disease.Nature medicine · 2023Article
- A Comprehensive Bioinformatics Approach to Identify Molecular Signatures and Key Pathways for the Huntington Disease.Bioinformatics and biology insights · 2023Article
- Divergent Effects of the Nonselective Adenosine Receptor Antagonist Caffeine in Pre-Manifest and Motor-Manifest Huntington's Disease.Biomedicines · 2022Article
- Emerging roles of dysregulated adenosine homeostasis in brain disorders with a specific focus on neurodegenerative diseases.Journal of biomedical science · 2021Review
- Molecular probes for the human adenosine receptors.Purinergic signalling · 2021Review
- Article
- Metabolic Aspects of Adenosine Functions in the Brain.Frontiers in pharmacology · 2021Review
- Purinergic Signaling in the Pathophysiology and Treatment of Huntington's Disease.Frontiers in neuroscience · 2021Review
- Huntington's Disease: A Review of the Known PET Imaging Biomarkers and Targeting Radiotracers.Molecules (Basel, Switzerland) · 2020Review
- Multiple clinical features of Huntington's disease correlate with mutant HTT gene CAG repeat lengths and neurodegeneration.Journal of neurology · 2019Review
- Clinical utility of FDG-PET in amyotrophic lateral sclerosis and Huntington's disease.European journal of nuclear medicine and molecular imaging · 2018Review
- The Role of Adenosine Tone and Adenosine Receptors in Huntington's Disease.Journal of caffeine and adenosine research · 2018Review
- Molecular Imaging Markers to Track Huntington's Disease Pathology.Frontiers in neurology · 2017Review
- Equilibrative nucleoside transporter ENT1 as a biomarker of Huntington disease.Neurobiology of disease · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeTo study cerebral adenosine receptors (AR) in premanifest and manifest stages of Huntington's disease (HD).
methodsWe quantified the cerebral binding potential (BP ND) of the A₁AR in carriers of the HD CAG trinucleotide repeat expansion using the radioligand [(18) F]CPFPX and PET. Four groups were investigated: (i) premanifest individuals far (preHD-A; n = 7) or (ii) near (preHD-B; n = 6) to the predicted symptom onset, (iii) manifest HD patients (n = 8), and (iv) controls (n = 36).
resultsCerebral A₁AR values of preHD-A subjects were generally higher than those of controls (by up to 31%, p < .01, in the thalamus on average). Across stages a successive reduction of A₁AR BPND was observed to the levels of controls in preHD-B and undercutting controls in manifest HD by down to 25%, p < .01, in the caudatus and amygdala. There was a strong correlation between A₁AR BP ND and years to onset. Before onset of HD, the assumed annual rates of change of A₁AR density were -1.2% in the caudatus, -1.7% in the thalamus and -3.4% in the amygdala, while the corresponding volume losses amounted to 0.6%, 0.1% and 0.2%, respectively.
conclusionsAdenosine receptors switch from supra to subnormal levels during phenoconversion of HD. This differential regulation may play a role in the pathophysiology of altered energy metabolism.
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.