title: Is Vasomotion in Cerebral Arteries Impaired in Alzheimer's Disease?
abstract: A substantial body of evidence supports the hypothesis of a vascular component in the pathogenesis of Alzheimer's disease (AD). Cerebral hypoperfusion and blood-brain barrier dysfunction have been indicated as key elements of this pathway. Cerebral amyloid angiopathy (CAA) is a cerebrovascular disorder, frequent in AD, characterized by the accumulation of amyloid-β (Aβ) peptide in cerebral blood vessel walls. CAA is associated with loss of vascular integrity, resulting in impaired regulation of cerebral circulation, and increased susceptibility to cerebral ischemia, microhemorrhages, and white matter damage. Vasomotion- the spontaneous rhythmic modulation of arterial diameter, typically observed in arteries/arterioles in various vascular beds including the brain- is thought to participate in tissue perfusion and oxygen delivery regulation. Vasomotion is impaired in adverse conditions such as hypoperfusion and hypoxia. The perivascular and glymphatic pathways of Aβ clearance are thought to be driven by the systolic pulse. Vasomotion produces diameter changes of comparable amplitude, however at lower rates, and could contribute to these mechanisms of Aβ clearance. In spite of potential clinical interest, studies addressing cerebral vasomotion in the context of AD/CAA are limited. This study reviews the current literature on vasomotion, and hypothesizes potential paths implicating impaired cerebral vasomotion in AD/CAA. Aβ and oxidative stress cause vascular tone dysregulation through direct effects on vascular cells, and indirect effects mediated by impaired neurovascular coupling. Vascular tone dysregulation is further aggravated by cholinergic deficit and results in depressed cerebrovascular reactivity and (possibly) impaired vasomotion, aggravating regional hypoperfusion and promoting further Aβ and oxidative stress accumulation.
authors.affiliation: Centre for Computational Imaging and Simulation Technologies in Biomedicine (CISTIB), Department of Electronic and Electrical Engineering, University of Sheffield, Sheffield, UK.
authors.forename: Luigi Yuri
authors.initials: LY
authors.lastname: Di Marco
authors.affiliation: Department of Medical Physics and Informatics, Faculty of Medicine and Faculty of Science and Informatics, University of Szeged, Szeged, Hungary.
authors.forename: Eszter
authors.initials: E
authors.lastname: Farkas
authors.affiliation: Department of Psychology, University of Sheffield, Sheffield, UK.
authors.forename: Chris
authors.initials: C
authors.lastname: Martin
authors.affiliation: Department of Neuroscience, University of Sheffield, Sheffield, UK.|IRCCS, Fondazione Ospedale S. Camillo, Venice, Italy.
authors.forename: Annalena
authors.initials: A
authors.lastname: Venneri
authors.affiliation: Centre for Computational Imaging and Simulation Technologies in Biomedicine (CISTIB), Department of Electronic and Electrical Engineering, University of Sheffield, Sheffield, UK.
authors.forename: Alejandro F
authors.initials: AF
authors.lastname: Frangi
mesh_terms: D000544:Alzheimer Disease / Q000150:complications* / Q000473:pathology*; D002539:Cerebral Arterial Diseases / Q000209:etiology*; D002536:Cerebral Arteries / Q000473:pathology / Q000503:physiopathology*; D006801:Humans; D014666:Vasomotor System / Q000503:physiopathology*
keywords: Alzheimer’s disease; cerebral amyloid angiopathy; cerebral autoregulation; endothelium; perivascular drainage; vascular smooth muscle cell; vasomotion