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Despite having few systemic vascular risk factors, individuals with Down syndrome have elevated cerebrovascular disease markers that track with the clinical progression of Alzheimer\u2019s disease, suggesting a role of cerebrovascular disease that is hypothesized to be mediated by inflammatory factors. This study examined the pathways through which small vessel cerebrovascular disease contributes to Alzheimer\u2019s disease-related pathophysiology and neurodegeneration in adults with Down syndrome. One hundred eighty-five participants from the Alzheimer\u2019s Biomarkers Consortium\u2013Down Syndrome [mean (SD) age = 45.2 (9.3) years] with available MRI and plasma biomarker data were included in this study. White matter hyperintensity (WMH) volumes were derived from T2-weighted fluid-attenuated inversion recovery MRI scans, and plasma biomarker concentrations of amyloid beta 42\/40, phosphorylated tau 217, astrocytosis (glial fibrillary acidic protein) and neurodegeneration (neurofilament light chain) were measured with ultrasensitive immunoassays. We examined the bivariate relationships of WMH, amyloid beta 42\/40, phosphorylated tau 217 and glial fibrillary acidic protein with age-residualized neurofilament light chain across Alzheimer\u2019s disease diagnostic groups. A series of mediation and path analyses examined statistical pathways linking WMH and Alzheimer\u2019s disease pathophysiology to promote neurodegeneration in the total sample and groups stratified by clinical diagnosis. There was a direct and indirect bidirectional effect through the glial fibrillary acidic protein of WMH on phosphorylated tau 217 concentration, which was associated with neurofilament light chain concentration in the entire sample. Amongst cognitively stable participants, WMH was directly and indirectly, through glial fibrillary acidic protein, associated with phosphorylated tau 217 concentration, and in those with mild cognitive impairment, there was a direct effect of WMH on phosphorylated tau 217 and neurofilament light chain concentrations. There were no associations of WMH with biomarker concentrations among those diagnosed with dementia. The findings from this cross-sectional study suggest that among individuals with Down syndrome, cerebrovascular disease promotes neurodegeneration by increasing astrocytosis and tau pathophysiology in the presymptomatic phases of Alzheimer\u2019s disease, but future studies will need to confirm these associations with longitudinal data. This work joins an emerging literature that implicates cerebrovascular disease and its interface with neuroinflammation as a core pathological feature of Alzheimer\u2019s disease in adults with Down syndrome.<\/jats:p>","DOI":"10.1093\/braincomms\/fcae331","type":"journal-article","created":{"date-parts":[[2024,9,24]],"date-time":"2024-09-24T15:23:14Z","timestamp":1727191394000},"source":"Crossref","is-referenced-by-count":25,"title":["Cerebrovascular disease is associated with Alzheimer\u2019s plasma biomarker concentrations in adults with Down syndrome"],"prefix":"10.1093","volume":"6","author":[{"given":"Natalie C","family":"Edwards","sequence":"first","affiliation":[{"name":"Taub Institute for Research on Alzheimer\u2019s Disease and the Aging Brain, Columbia University , New York City, NY 10032 ,","place":["USA"]},{"name":"Department of Neurology, Vagelos College of Physicians and Surgeons, Columbia University , New York City, NY 10032 ,","place":["USA"]},{"name":"Department of 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