ArticleJournal of neuroscience research2017
Sex-specific effects of the Huntington gene on normal neurodevelopment.
Article in Journal of neuroscience research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
What it found
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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.
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Who cites it
36 citing papers in PubMed, 52 citations in OpenAlex.
- Effect of Trinucleotide Repeats in the Huntington's Gene on Intelligence.EBioMedicine · 2018Trial
- Sex-related differences in Huntington's disease: a scoping review.Biology of sex differences · 2026Article
- Observational
- Buried Treasure? Overlooked and Newly Discovered Evolutionary Contributions to Human Brain Diseases.Annals of neurology · 2025Review
- Childhood to Adult Neurodevelopment in Gene-Expanded Huntington's Disease (ChANGE-HD) study protocol: A Prospective Longitudinal Neurodevelopmental Study of Huntington's Disease.medRxiv : the preprint server for health sciences · 2025Article
- The HTT gene influences plasma neurofilament light chain and brain metabolism in prodromal Alzheimer's disease.Journal of neurology · 2025Article
- Huntingtin CAG repeat size variations below the Huntington's disease threshold: associations with depression, anxiety and basal ganglia structure.European journal of human genetics : EJHG · 2025Article
- Mutant Huntingtin Drives Development of an Advantageous Brain Early in Life: Evidence in Support of Antagonistic Pleiotropy.Annals of neurology · 2024Article
- Unravelling the role of huntingtin: from neurodevelopment to neurodegeneration.Brain : a journal of neurology · 2023Article
- Article
- Gender differences in cognitive reserve: implication for subjective cognitive decline in women.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2022Article
- A Progressive Loss of phosphoSer138-Profilin Aligns with Symptomatic Course in the R6/2 Mouse Model of Huntington's Disease: Possible Sex-Dependent Signaling.Cellular and molecular neurobiology · 2022Article
- The evolutionary history of the polyQ tract in huntingtin sheds light on its functional pro-neural activities.Cell death and differentiation · 2022Article
- CAG Repeats Within the Non-pathological Range in the HTT Gene Influence Personality Traits in Patients With Subjective Cognitive Decline: A 13-Year Follow-Up Study.Frontiers in psychiatry · 2022Article
- Metacognitive insight into cognitive performance in Huntington's disease gene carriers.BMJ neurology open · 2022Article
- Interaction between sex and neurofilament light chain on brain structure and clinical severity in Huntington's disease.Annals of clinical and translational neurology · 2021Article
- The Effect of CAG Repeats within the Non-Pathological Range in the HTT Gene on Cognitive Functions in Patients with Subjective Cognitive Decline and Mild Cognitive Impairment.Diagnostics (Basel, Switzerland) · 2021Article
- Effects of mutant huntingtin inactivation on Huntington disease-related behaviours in the BACHD mouse model.Neuropathology and applied neurobiology · 2021Article
- Association of CAG Repeat Length in the Huntington Gene With Cognitive Performance in Young Adults.Neurology · 2021Article
- Neurodevelopmental disorders: 2021 update.Free neuropathology · 2021Article
Corrections and comments
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Authors and funding
14 authors at 5 institutions in 2 countries.
Funding
Abstract
Huntington disease is a neurodegenerative disorder caused by a gene (HTT) with a unique feature of trinucleotide repeats ranging from 10 to 35 in healthy people; when expanded beyond 39 repeats, Huntington disease develops. Animal models demonstrate that HTT is vital to brain development; however, this has not been studied in humans. Moreover, evidence suggests that triplet repeat genes may have been vital in evolution of the human brain. Here we evaluate brain structure using magnetic resonance imaging and brain function using cognitive tests in a sample of school-aged children ages 6 to 18 years old. DNA samples were processed to quantify the number of CAG repeats within HTT. We find that the number of repeats in HTT, below disease threshold, confers advantageous changes in brain structure and general intelligence (IQ): the higher the number of repeats, the greater the change in brain structure, and the higher the IQ. The pattern of structural brain changes associated with HTT is strikingly different between males and females. HTT may confer an advantage or a disadvantage depending on the repeat length, playing a key role in either the evolution of a superior human brain or development of a uniquely human brain disease. © 2016 Wiley Periodicals, Inc.
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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.