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Fox Foundation for Parkinson\u2019s Research","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000864","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2024,3,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Cerebrovascular pathology often co-exists with Alzheimer\u2019s disease pathology and can contribute to Alzheimer\u2019s disease-related clinical progression. However, the degree to which vascular burden contributes to Alzheimer\u2019s disease pathological progression is still unclear. This study aimed to investigate interactions between vascular burden and amyloid-\u03b2 pathology on both baseline tau tangle load and longitudinal tau accumulation.<\/jats:p>\n               <jats:p>We included 1229 participants from the Swedish BioFINDER-2 Study, including cognitively unimpaired and impaired participants with and without biomarker-confirmed amyloid-\u03b2 pathology. All underwent baseline tau-PET (18F-RO948), and a subset (n = 677) underwent longitudinal tau-PET after 2.5 \u00b1 1.0\u2005years. Tau-PET uptake was computed for a temporal meta-region-of-interest. We focused on four main vascular imaging features and risk factors: microbleeds; white matter lesion volume; stroke-related events (infarcts, lacunes and haemorrhages); and the Framingham Heart Study Cardiovascular Disease risk score. To validate our in vivo results, we examined 1610 autopsy cases from an Arizona-based neuropathology cohort on three main vascular pathological features: cerebral amyloid angiopathy; white matter rarefaction; and infarcts. For the in vivo cohort, primary analyses included age-, sex- and APOE \u025b4-corrected linear mixed models between tau-PET (outcome) and interactions between time, amyloid-\u03b2 and each vascular feature (predictors). For the neuropathology cohort, age-, sex- and APOE \u025b4-corrected linear models between tau tangle density (outcome) and an interaction between plaque density and each vascular feature (predictors) were performed.<\/jats:p>\n               <jats:p>In cognitively unimpaired individuals, we observed a significant interaction between microbleeds and amyloid-\u03b2 pathology on greater baseline tau load (\u03b2 = 0.68, P &amp;lt; 0.001) and longitudinal tau accumulation (\u03b2 = 0.11, P &amp;lt; 0.001). For white matter lesion volume, we did not observe a significant independent interaction effect with amyloid-\u03b2 on tau after accounting for microbleeds. In cognitively unimpaired individuals, we further found that stroke-related events showed a significant negative interaction with amyloid-\u03b2 on longitudinal tau (\u03b2 = \u22120.08, P &amp;lt; 0.001). In cognitively impaired individuals, there were no significant interaction effects between cerebrovascular and amyloid-\u03b2 pathology at all. In the neuropathology dataset, the in vivo observed interaction effects between cerebral amyloid angiopathy and plaque density (\u03b2 = 0.38, P &amp;lt; 0.001) and between infarcts and plaque density (\u03b2 = \u22120.11, P = 0.005) on tau tangle density were replicated.<\/jats:p>\n               <jats:p>To conclude, we demonstrated that cerebrovascular pathology\u2014in the presence of amyloid-\u03b2 pathology\u2014modifies tau accumulation in early stages of Alzheimer\u2019s disease. More specifically, the co-occurrence of microbleeds and amyloid-\u03b2 pathology was associated with greater accumulation of tau aggregates during early disease stages. This opens the possibility that interventions targeting microbleeds may attenuate the rate of tau accumulation in Alzheimer\u2019s disease.<\/jats:p>","DOI":"10.1093\/brain\/awad317","type":"journal-article","created":{"date-parts":[[2023,9,17]],"date-time":"2023-09-17T12:17:07Z","timestamp":1694953027000},"page":"949-960","source":"Crossref","is-referenced-by-count":48,"title":["Interactions between vascular burden and amyloid-\u03b2 pathology on trajectories of tau accumulation"],"prefix":"10.1093","volume":"147","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-4289-9101","authenticated-orcid":false,"given":"Emma M","family":"Coomans","sequence":"first","affiliation":[{"name":"Radiology and Nuclear Medicine, Vrije Universiteit Amsterdam, Amsterdam UMC location VUmc , 1081HV Amsterdam , The Netherlands"},{"name":"Amsterdam Neuroscience, Brain Imaging , 1081HV Amsterdam , The Netherlands"},{"name":"Clinical Memory Research Unit, Department of Clinical Sciences Malm\u00f6, Lund 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