Trial reportEBioMedicine2018
Effect of Trinucleotide Repeats in the Huntington's Gene on Intelligence.
Trial report in EBioMedicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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
35 citing papers in PubMed, 54 citations in OpenAlex.
- Performance Evaluation of PacBio PureTarget for Multiple Short Tandem Repeat Expansion Detection.Annals of laboratory medicine · 2026Article
- Review
- Higher educational attainment in Huntington disease families: evidence from the Enroll-HD study.Orphanet journal of rare diseases · 2026Article
- Gene therapy for huntington's disease: advances, challenges, and future perspectives.Neurogenetics · 2026Review
- Lifetime risk of cancer in carriers of intermediate alleles in the HTT gene.Scientific reports · 2026Article
- Sequence Variants in Small CAG Repeat Expansions of theNeurology · 2026Article
- Observational
- Genetic Profiling of Huntington's Disease: Insights from CAG Repeat Analysis for Precision Diagnosis and Management.Noro psikiyatri arsivi · 2026Article
- Movement disorders: a brief overview from an evolutionary perspective.Journal of neural transmission (Vienna, Austria : 1996) · 2025Review
- Review
- When repetita no-longer iuvant: somatic instability of the CAG triplet in Huntington's disease.Nucleic acids research · 2025Review
- Mutant Huntingtin Drives Development of an Advantageous Brain Early in Life: Evidence in Support of Antagonistic Pleiotropy.Annals of neurology · 2024Article
- Neurodegenerative Diseases: New Hopes and Perspectives.Current molecular medicine · 2024Review
- Article
- An Overview of the Pathophysiological Mechanisms of 3-Nitropropionic Acid (3-NPA) as a Neurotoxin in a Huntington's Disease Model and Its Relevance to Drug Discovery and Development.Neurochemical research · 2023Review
- STRling: a k-mer counting approach that detects short tandem repeat expansions at known and novel loci.Genome biology · 2022Article
- The distribution and density of Huntingtin inclusions across the Huntington disease neocortex: regional correlations with Huntingtin repeat expansion independent of pathologic grade.Acta neuropathologica communications · 2022Article
- The evolutionary history of the polyQ tract in huntingtin sheds light on its functional pro-neural activities.Cell death and differentiation · 2022Article
- Extreme conservation of the poly-glutamine tract in huntingtin is related to neurodevelopmental functions: the "better" may become the "enemy of the good" in the course of evolution.Cell death and differentiation · 2022Article
- Cortical Features in Child and Adolescent Carriers of Mutant Huntingtin (mHTT).Journal of Huntington's disease · 2022Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
backgroundHuntington's Disease (HD) is caused by an abnormality in the HTT gene. This gene includes trinucleotide repeats ranging from 10 to 35, and when expanded beyond 39, causes HD. We previously reported that CAG repeats in the normal range had a direct and beneficial effect on brain development with higher repeats being associated with higher cognitive function. The current study now expands this line of inquiry to evaluate the effects of CAG repeat throughout the entire spectrum of repeats from 15 to 58.
methodsWe evaluated brain function in children ages 6-18 years old. DNA samples were processed to quantify the number of CAG repeats within HTT. Linear regression was used to determine if number of CAG repeats predicted measures of brain function.
findingsThe number of repeats in HTT, had a non-linear effect on a measure of general intelligence with an inverted U shape pattern. Increasing repeat length was associated with higher GAI scores up until roughly 40-41 repeats. After this peak, increasing repeat length was associated with declining GAI scores.
interpretationHTT may confer an advantage or a disadvantage depending upon the repeat length, playing a key role in the determination of intelligence, or causing a uniquely human brain disease.
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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.