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Individuals with \u226540 cytosine\u2013adenine\u2013guanine repeats on the interesting transcript 15 gene develop Huntington\u2019s 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\u2019s disease. However, a non-invasive assessment of neurovascular unit function in Huntington\u2019s disease has not yet been performed. Here, we investigate neurovascular interactions in presymptomatic (N = 13) and symptomatic (N = 15) Huntington\u2019s disease participants compared to healthy controls (N = 36). To assess the dynamics of oxygen transport to the brain, functional near-infrared spectroscopy, ECG and respiration effort were recorded. Simultaneously, neuronal activity was assessed using EEG. The resultant time series were analysed using methods for discerning time-resolved multiscale dynamics, such as wavelet transform power and wavelet phase coherence. Neurovascular phase coherence in the interval around 0.1\u2005Hz is significantly reduced in both Huntington\u2019s disease groups. The presymptomatic Huntington\u2019s disease group has a lower power of oxygenation oscillations compared to controls. The spatial coherence of the oxygenation oscillations is lower in the symptomatic Huntington\u2019s disease group compared to the controls. The EEG phase coherence, especially in the \u03b1 band, is reduced in both Huntington\u2019s disease groups and, to a significantly greater extent, in the symptomatic group. Our results show a reduced efficiency of the neurovascular unit in Huntington\u2019s disease both in the presymptomatic and symptomatic stages of the disease. The vasculature is already significantly impaired in the presymptomatic stage of the disease, resulting in reduced cerebral blood flow control. The results indicate vascular remodelling, which is most likely a compensatory mechanism. In contrast, the declines in \u03b1 and \u03b3 coherence indicate a gradual deterioration of neuronal activity. The results raise the question of whether functional changes in the vasculature precede the functional changes in neuronal activity, which requires further investigation. The observation of altered dynamics paves the way for a simple method to monitor the progression of Huntington\u2019s disease non-invasively and evaluate the efficacy of treatments.<\/jats:p>","DOI":"10.1093\/braincomms\/fcae166","type":"journal-article","created":{"date-parts":[[2024,6,10]],"date-time":"2024-06-10T00:02:57Z","timestamp":1717977777000},"source":"Crossref","is-referenced-by-count":13,"title":["The phase coherence of the neurovascular unit is reduced in Huntington\u2019s disease"],"prefix":"10.1093","volume":"6","author":[{"given":"Juliane","family":"Bjerkan","sequence":"first","affiliation":[{"name":"Department of Physics, Lancaster University , Lancaster LA1 4YB , UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jan","family":"Kobal","sequence":"additional","affiliation":[{"name":"Department of Neurology, University Medical Centre , 1525 Ljubljana , Slovenia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gemma","family":"Lancaster","sequence":"additional","affiliation":[{"name":"Department of Physics, Lancaster University , Lancaster LA1 4YB , UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sanja","family":"\u0160e\u0161ok","sequence":"additional","affiliation":[{"name":"Department of Neurology, University Medical Centre , 1525 Ljubljana , Slovenia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bernard","family":"Megli\u010d","sequence":"additional","affiliation":[{"name":"Department of Neurology, University Medical Centre , 1525 Ljubljana , Slovenia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Peter V E","family":"McClintock","sequence":"additional","affiliation":[{"name":"Department of Physics, Lancaster University , Lancaster LA1 4YB , UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Karol P","family":"Budohoski","sequence":"additional","affiliation":[{"name":"Division of Neurosurgery, Department of Clinical Neurosciences, Addenbrooke's Hospital, University of Cambridge , Cambridge CB2 0QQ , UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Peter J","family":"Kirkpatrick","sequence":"additional","affiliation":[{"name":"Division of Neurosurgery, Department of Clinical Neurosciences, Addenbrooke's Hospital, University of Cambridge , Cambridge CB2 0QQ , UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6952-8370","authenticated-orcid":false,"given":"Aneta","family":"Stefanovska","sequence":"additional","affiliation":[{"name":"Department of Physics, Lancaster University , Lancaster LA1 4YB , 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