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Blood-brain barrier integrity is linked to cognitive function, but not to cerebral arterial pulsatility, among elderly
Umeå University, Faculty of Medicine, Department of Diagnostics and Intervention. Umeå University, Faculty of Science and Technology, Department of Applied Physics and Electronics. Department of Medical Physics, School of Medicine and Public Health, University of Wisconsin-Madison, WI, Madison, United States.ORCID iD: 0000-0003-3181-785X
Umeå University, Faculty of Medicine, Department of Diagnostics and Intervention.ORCID iD: 0000-0002-0532-232X
Umeå University, Faculty of Medicine, Department of Diagnostics and Intervention.
Umeå University, Faculty of Medicine, Department of Diagnostics and Intervention. Umeå University, Faculty of Medicine, Umeå Centre for Functional Brain Imaging (UFBI). Umeå University, Faculty of Medicine, Department of Medical and Translational Biology.ORCID iD: 0000-0002-3367-1746
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2024 (English)In: Scientific Reports, E-ISSN 2045-2322, Vol. 14, no 1, article id 15338Article in journal (Refereed) Published
Abstract [en]

Blood-brain barrier (BBB) disruption may contribute to cognitive decline, but questions remain whether this association is more pronounced for certain brain regions, such as the hippocampus, or represents a whole-brain mechanism. Further, whether human BBB leakage is triggered by excessive vascular pulsatility, as suggested by animal studies, remains unknown. In a prospective cohort (N = 50; 68-84 years), we used contrast-enhanced MRI to estimate the permeability-surface area product (PS) and fractional plasma volume ( formula presented ), and 4D flow MRI to assess cerebral arterial pulsatility. Cognition was assessed by the Montreal Cognitive Assessment (MoCA) score. We hypothesized that high PS would be associated with high arterial pulsatility, and that links to cognition would be specific to hippocampal PS. For 15 brain regions, PS ranged from 0.38 to 0.85 (·10-3 min-1) and formula presented from 0.79 to 1.78%. Cognition was related to PS (·10-3 min-1) in hippocampus (β = - 2.9; p = 0.006), basal ganglia (β = - 2.3; p = 0.04), white matter (β = - 2.6; p = 0.04), whole-brain (β = - 2.7; p = 0.04) and borderline-related for cortex (β = - 2.7; p = 0.076). Pulsatility was unrelated to PS for all regions (p > 0.19). Our findings suggest PS-cognition links mainly reflect a whole-brain phenomenon with only slightly more pronounced links for the hippocampus, and provide no evidence of excessive pulsatility as a trigger of BBB disruption.

Place, publisher, year, edition, pages
Springer Nature, 2024. Vol. 14, no 1, article id 15338
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Neurosciences
Identifiers
URN: urn:nbn:se:umu:diva-227865DOI: 10.1038/s41598-024-65944-yPubMedID: 38961135Scopus ID: 2-s2.0-85197675960OAI: oai:DiVA.org:umu-227865DiVA, id: diva2:1884923
Funder
Swedish Research Council, 2022-04263Swedish Heart Lung Foundation, 20210653Swedish Foundation for Strategic ResearchThe Kempe FoundationsAvailable from: 2024-07-19 Created: 2024-07-19 Last updated: 2024-07-19Bibliographically approved

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Vikner, TomasGarpebring, AndersBjörnfot, CeciliaNyberg, LarsMalm, JanEklund, AndersWåhlin, Anders

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Vikner, TomasGarpebring, AndersBjörnfot, CeciliaNyberg, LarsMalm, JanEklund, AndersWåhlin, Anders
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Department of Diagnostics and InterventionDepartment of Applied Physics and ElectronicsUmeå Centre for Functional Brain Imaging (UFBI)Department of Medical and Translational BiologyNeurosciences
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