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One notable alteration is an enrichment of terminal sialic acid (SA) modifications. Previous studies provide evidence of increased sialylation on microglia, the innate immune cell of the brain, in Alzheimer's disease (AD), particularly near amyloid beta plaques. Yet, there is little understanding of the relationship between SA and other amyloid beta\u2010related diseases like Cerebral Amyloid Angiopathy (CAA). Nearly half of all AD cases have CAA; thus, it is critical to understand the relationship between amyloid pathology and SA modifications. The present study aimed to overcome this gap in knowledge by investigating sialylation patterns in AD cases with CAA compared with CAA\u2010negative AD cases and amyloid\u2010negative control cases. The localization of SA modifications was investigated in the frontal cortex of 30 post\u2010mortem cases with or without diagnoses of AD and\/or CAA. Quantitative digital pathology analyses were used to determine regional SA differences in parenchymal and leptomeningeal blood vessels. First, we found no difference in intravascular amyloid\u2010beta levels between the parenchymal and leptomeningeal vessels of AD with CAA cases, suggesting no regional differences in this amyloid aggregation. Next, there was a visual increase in microglia sialylation surrounding parenchymal blood vessels in the CAA cases. Notably, there were significant differences in intravascular SA levels across the three comparison groups. AD cases with CAA had significantly greater sialylation levels in both the parenchymal and leptomeningeal vessels compared with the AD\u2010only and control groups. This is a novel finding that supports the consideration of glycosylation changes that contribute to worse pathological outcomes in AD with CAA.<\/jats:p>","DOI":"10.1111\/bpa.70042","type":"journal-article","created":{"date-parts":[[2025,9,17]],"date-time":"2025-09-17T04:56:22Z","timestamp":1758084982000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["Sialylation patterns in cerebral amyloid angiopathy"],"prefix":"10.1111","volume":"36","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-4729-2712","authenticated-orcid":false,"given":"Caitlyn","family":"Fastenau","sequence":"first","affiliation":[{"name":"Glenn Biggs Institute for Alzheimer's &amp; Neurodegenerative Diseases University of Texas Health Science Center at San Antonio  San Antonio Texas USA"},{"name":"Department of Pharmacology University of Texas Health Science Center at San Antonio  San Antonio Texas 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