ArticleBrain communications2024
The phase coherence of the neurovascular unit is reduced in Huntington's disease.
Article in Brain communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Dysfunction of the neurovascular unit as a temporal driver in Alzheimer's pathogenesis.Translational neurodegeneration · 2026Review
- Modelling brain metabolism with interacting nonautonomous phase oscillators.Frontiers in network physiology · 2026Article
- BA9 Transcriptomics in Huntington's Disease 80-Gene Signature and MIR219A2-Linked Targets.International journal of molecular sciences · 2025Article
- Neural Correlates of Huntington's Disease Based on Electroencephalography (EEG): A Mechanistic Review and Discussion of Excitation and Inhibition (E/I) Imbalance.Journal of clinical medicine · 2025Review
- A valuation based theory of learning's origin and development.Frontiers in systems neuroscience · 2025Article
- Neurovascular phase coherence is altered in Alzheimer's disease.Brain communications · 2025Article
- Review
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Huntington's disease is a neurodegenerative disorder in which neuronal death leads to chorea and cognitive decline. Individuals with ≥40 cytosine-adenine-guanine repeats on the interesting transcript 15 gene develop Huntington's disease due to a mutated huntingtin protein. While the associated structural and molecular changes are well characterized, the alterations in neurovascular function that lead to the symptoms are not yet fully understood. Recently, the neurovascular unit has gained attention as a key player in neurodegenerative diseases. The mutant huntingtin protein is known to be present in the major parts of the neurovascular unit in individuals with Huntington's disease. However, a non-invasive assessment of neurovascular unit function in Huntington's disease has not yet been performed. Here, we investigate neurovascular interactions in presymptomatic (
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