Brain Deep Medullary Veins on 7T MRI in Dutch-Type Hereditary Cerebral Amyloid Angiopathy
BACKGROUND: Deep medullary vein (DMV) changes occur in cerebral small vessel diseases (SVD) and in Alzheimer's disease. Cerebral amyloid angiopathy (CAA) is a common SVD that has a high co-morbidity with Alzheimer's disease. So far, DMVs have not been evaluated in CAA. OBJECTIVE: To evaluate DMVs in Dutch-type hereditary CAA (D-CAA) mutation carriers and controls, in relation to MRI markers associated with D-CAA. METHODS: Quantitative DMV parameters length, tortuosity, inhomogeneity, and density were quantified on 7 Tesla 3D susceptibility weighted MRI in pre-symptomatic D-CAA mutation carrier... Mehr ...
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Dokumenttyp: | Artikel |
Erscheinungsdatum: | 2022 |
Schlagwörter: | Cerebral small vessel disease / cerebral veins / hereditary cerebral amyloid angiopathy / magnetic resonance imaging / Brain/diagnostic imaging / Cerebral Amyloid Angiopathy/diagnostic imaging / Humans / Cerebral Hemorrhage/diagnostic imaging / Cerebral Amyloid Angiopathy / Familial/diagnostic imaging / Magnetic Resonance Imaging/methods / Alzheimer Disease/complications / Diffusion Tensor Imaging / Geriatrics and Gerontology / Psychiatry and Mental health / Clinical Psychology / General Neuroscience / Research Support / Non-U.S. Gov't / Journal Article / N.I.H. / Extramural |
Sprache: | Englisch |
Permalink: | https://search.fid-benelux.de/Record/base-27457805 |
Datenquelle: | BASE; Originalkatalog |
Powered By: | BASE |
Link(s) : | https://dspace.library.uu.nl/handle/1874/447809 |
BACKGROUND: Deep medullary vein (DMV) changes occur in cerebral small vessel diseases (SVD) and in Alzheimer's disease. Cerebral amyloid angiopathy (CAA) is a common SVD that has a high co-morbidity with Alzheimer's disease. So far, DMVs have not been evaluated in CAA. OBJECTIVE: To evaluate DMVs in Dutch-type hereditary CAA (D-CAA) mutation carriers and controls, in relation to MRI markers associated with D-CAA. METHODS: Quantitative DMV parameters length, tortuosity, inhomogeneity, and density were quantified on 7 Tesla 3D susceptibility weighted MRI in pre-symptomatic D-CAA mutation carriers (n = 8), symptomatic D-CAA mutation carriers (n = 8), and controls (n = 25). Hemorrhagic MRI markers (cerebral microbleeds, intracerebral hemorrhages, cortical superficial siderosis, convexity subarachnoid hemorrhage), non-hemorrhagic MRI markers (white matter hyperintensities, enlarged perivascular spaces, lacunar infarcts, cortical microinfarcts), cortical grey matter perfusion, and diffusion tensor imaging parameters were assessed in D-CAA mutation carriers. Univariate general linear analysis was used to determine associations between DMV parameters and MRI markers. RESULTS: Quantitative DMV parameters length, tortuosity, inhomogeneity, and density did not differ between pre-symptomatic D-CAA mutation carriers, symptomatic D-CAA mutation carriers, and controls. No associations were found between DMV parameters and MRI markers associated with D-CAA. CONCLUSION: This study indicates that vascular amyloid-β deposition does not affect DMV parameters. In patients with CAA, DMVs do not seem to play a role in the pathogenesis of MRI markers associated with CAA.