Blood‐brain barrier disruption measured by dynamic contrast‐enhanced MRI in Alzheimer’s disease
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Le résumé fourni par la source
Abstract Background Alzheimer’s disease (AD) is characterized by the accumulation of amyloid beta (Aβ) plaques in the brain. Blood‐brain barrier (BBB) dysfunction has been associated with AD. Aβ‐plaques have been found to disrupt the BBB, leading to increased permeability and invasion of immune cells into the CNS and triggering an inflammatory response, and contributing to neurodegeneration. In this study, we investigated BBB disruption in Alzheimer’s disease and its associations with amyloid deposition and clinical severity, and cognitive decline. Method In this cross‐sectional study, n = 16 AD patients were included. AD patients were defined as amyloid positive by CSF amyloid‐β42/amyloid‐β40 ratio < 5,5% and a Mini‐Mental‐State Examination (MMSE) score < 27. Dynamic contrast‐enhanced magnetic resonance imaging (DCE MRI), a non‐invasive imaging technique that uses intravenously injected gadolinium to quantify the permeability of the BBB has been acquired. DCE‐MRI quantification was quantified using the Patlak method. To analyse the regional degree of BBB disruption the AAL atlas was warped onto the Patlak maps and the median of each ROI was calculated. The cortical amyloid deposition has been quantified using 18F]flutemetamol β‐amyloid‐PET and cognitive performance was assessed using the Alzheimer’s Disease neuropsychological battery (CERAD‐NB). Associations were tested using linear regression models adjusted for age and sex in SPSS. Result The highest Ktrans values were measured in the orbitofrontal cortex (mean: 1,6×10−3 min−1). BBB dysfunction in median Ktrans values in the bilateral temporal lobe and particularly the right hippocampus were associated with decreases in the CSF amyloid‐β ratio. Furthermore, BBB dysfunction was negatively associated with cognitive decline measured by the CERAD‐NB. BBB dysfunction overlapped with amyloid PET accumulation in the parietal and temporal brain regions. Conclusion DCE MRI shows spatially localized BBB dysfunction in AD. The BBB dysfunction seems to be more severe in regions of the brain that are affected by Aβ plaques. This could support the idea that Aβ plaque contributes to BBB dysfunction in AD. BBB dysfunction also tends to be pronounced in patients with more severe cognitive impairment, suggesting that it may play a role in the progression of AD.
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Le contrôle bibliographique ouvert
DOI retrouvé dans Crossref DOI retrouvé ; titre concordant.
- Titre Crossref
- Blood‐brain barrier disruption measured by dynamic contrast‐enhanced MRI in Alzheimer’s disease
- Date Crossref
- 01/12/2023
- Éditeur
- Wiley
- Type
- journal-article
Ce recoupement confirme des métadonnées liées au DOI. Il ne confirme ni la méthode ni les conclusions de l’étude, et il ne compte pas comme une seconde source scientifique indépendante.
Où se fait cette recherche
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German Center for Neurodegenerative Diseases pays non établi dans la noticeStructure de recherche
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LMU Klinikum pays non établi dans la noticeÉtablissement de santé
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Ludwig-Maximilians-Universität München pays non établi dans la noticeUniversité ou école supérieure
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University of Sheffield Sheffield Institute for Translational Neuroscience pays non établi dans la noticeUniversité ou école supérieure
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Munich Cluster for Systems Neurology pays non établi dans la noticeStructure de recherche
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Stroke Association pays non établi dans la noticeOrganisation à but non lucratif
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Institut für Schlaganfall- und Demenzforschung pays non établi dans la noticeUniversité ou école supérieure
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Imperial College London pays non établi dans la noticeUniversité ou école supérieure
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University Hospital Department of Psychiatry and Psychotherapy pays non établi dans la noticeUniversité ou école supérieure
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Institute for Stroke and Dementia Research pays non établi dans la noticeStructure de recherche
German Center for Neurodegenerative Diseases, LMU Klinikum et Ludwig-Maximilians-Universität München, avec 7 autres affiliations.
Une affiliation ne permet pas de déduire la nationalité d’un auteur.