ArticleAutonomic neuroscience : basic & clinical2021
Autonomic dysregulation as an early pathologic feature of Huntington Disease.
Article in Autonomic neuroscience : basic & clinical, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.
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Who cites it
12 citing papers in PubMed, 1 synthesis or guideline pooled it, 18 citations in OpenAlex.
- Systemic Symptoms in Huntington's Disease: A Comprehensive Review.Movement disorders clinical practice · 2024Pooled it
- Observational
- Circadian rhythms are disrupted in patients and preclinical models of Machado-Joseph disease.Brain : a journal of neurology · 2025Article
- Autonomic dysfunction in neurodegenerative disease.Nature reviews. Neuroscience · 2025Review
- The microbiota-gut-brain axis in Huntington's disease: pathogenic mechanisms and therapeutic targets.The FEBS journal · 2025Review
- Mutant Huntingtin Drives Development of an Advantageous Brain Early in Life: Evidence in Support of Antagonistic Pleiotropy.Annals of neurology · 2024Article
- Review
- Modulation of the Circadian Rhythm and Oxidative Stress as Molecular Targets to Improve Vascular Dementia: A Pharmacological Perspective.International journal of molecular sciences · 2024Review
- The phase coherence of the neurovascular unit is reduced in Huntington's disease.Brain communications · 2024Article
- Circadian and ultradian rhythms in normal mice and in a mouse model of Huntington's disease.Chronobiology international · 2022Article
- Autonomic changes in Huntington's disease correlate with altered central autonomic network connectivity.Brain communications · 2022Article
- Defining circadian disruption in neurodegenerative disorders.The Journal of clinical investigation · 2021Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveAutonomic nervous system (ANS) dysfunction has been described in adults with motor-manifest Huntington's Disease (HD) or those who are near their predicted motor onset. It is unclear if ANS dysfunction is present years prior to the onset of motor symptoms of HD. To bridge this gap in knowledge, we compared crude markers of ANS function between children with the gene-expansion that causes HD (GE group) who were decades from their predicted motor onset and gene-non-expanded children (GNE group).
methodsWe included participants from the Kids-HD study who were <18 years old. Linear mixed effects regression models were constructed that controlled for sex, age, and BMI, and included a random effect per participant and per family. We compared resting heart rate (rHR), core body temperature (CBT), systolic blood pressure (SBP), and diastolic blood pressure (DBP) between the GE (n = 84) and GNE (n = 238) groups. We then grouped participants from the GE group based on their predicted years to onset (YTO) and compared their vital signs to the GNE group.
resultsThe GE group had higher rHR (∆ = 3.83, p = 0.0064), SBP (∆ = 2.38, p = 0.032), and CBT (∆ = 0.16, t = 2.92, p = 0.007). The mean rHR and CBT became significantly elevated compared to the GNE group in participants who had 15-25 YTO and those who had <15 YTO. The mean SBP of participants who had 25-35 YTO was significantly elevated compared to the GNE group.
conclusionANS dysfunction in HD seems to occur approximately 20 years prior to the predicted onset of motor symptoms of HD.
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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 Socratic graph.