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could improve our understanding of underlying biological pathways leading to vascular brain injury (VBI) and neurodegeneration.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>To identify plasma protein markers of MRI markers of VBI and amyloid- and tau-PET burden in cognitively healthy adults.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      125 plasma proteins were measured in dementia-free Framingham third Generation cohort participants between 2002\u20132005 (mean age 46 [SD 8]) with available MRI brain (n\u2009=\u20091039),\n                      <jats:sup>11<\/jats:sup>\n                      C-Pittsburgh Compound-B (PiB)- (n\u2009=\u2009279), and\/or\n                      <jats:sup>18<\/jats:sup>\n                      F-Flortaucipir (FTP)-PET (n\u2009=\u2009239) performed \u223c13\u201315 years after blood sampling. Outcomes included white matter hyperintensities, peak width of skeletonized mean diffusivity, and free water); precuneus-, posterior cingulate- and frontal, lateral and retrosplenial cortices-A\u03b2 deposition; and global- and entorhinal cortex-tau.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Growth differentiation factor-15 (GDF-15) was associated with increased VBI (p\u2009\u2264\u20090.02), while soluble receptor for advanced glycation end products (sRAGE) and insulin-like growth factor 1 (IGF-1) were associated with reduced VBI (p\u2009\u2264\u20090.04). Plasma tau, renin, and ApoB were associated with increased A\u03b2 deposition (p\u2009\u2264\u20090.02), while sRAGE was associated with reduced A\u03b2 deposition in all regions (p\u2009\u2264\u20090.03). Brain natriuretic peptide (NT-proBNP) and purine nucleoside phosphorylase (PNP) were associated with increased tau deposition (p\u2009\u2264\u20090.02), while low density lipoprotein cholesterol (LDL-C) and GDF-15 were associated with reduced tau deposition (p\u2009\u2264\u20090.04).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Candidate vascular plasma proteins measured in dementia-free, asymptomatic adults at late mid-life were associated with subsequent neuroimaging markers of VBI and tau and amyloid deposition. Our findings highlight potential novel candidate vascular biomarkers for preclinical dementia but will require validation.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1177\/13872877261480733","type":"journal-article","created":{"date-parts":[[2026,8,31]],"date-time":"2026-08-31T03:28:11Z","timestamp":1788146891000},"page":"1674-1699","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":0,"title":["Mid-life candidate vascular plasma biomarkers are associated with MRI markers of vascular brain injury and amyloid- and tau-PET in cognitively healthy adults"],"prefix":"10.1177","volume":"113","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-2042-257X","authenticated-orcid":false,"given":"Martin D.","family":"Mulligan","sequence":"first","affiliation":[{"name":"University of Galway"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ruiqi","family":"Wang","sequence":"additional","affiliation":[{"name":"The Framingham Heart Study, Framingham, MA, USA"},{"name":"Boston University School of Public Health"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qiong","family":"Yang","sequence":"additional","affiliation":[{"name":"The Framingham Heart Study, Framingham, MA, USA"},{"name":"Boston University School of Public Health"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alexa S.","family":"Beiser","sequence":"additional","affiliation":[{"name":"The Framingham Heart Study, Framingham, MA, USA"},{"name":"Boston University School of Public Health"},{"name":"Boston University Chobanian & Avedisian School of Medicine"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3516-6345","authenticated-orcid":false,"given":"Pauline","family":"Maillard","sequence":"additional","affiliation":[{"name":"Department of Neurology, UC Davis School of Medicine, Sacramento, CA, USA"},{"name":"University of California, Davis"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1115-4430","authenticated-orcid":false,"given":"Claudia","family":"Satizabal","sequence":"additional","affiliation":[{"name":"The Framingham Heart Study, Framingham, MA, USA"},{"name":"Boston University Chobanian & Avedisian School of Medicine"},{"name":"Glenn Biggs Institute for Alzheimer's &amp; Neurodegenerative Diseases, University of Texas Health Sciences Center, San Antonio, TX, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Saptaparni","family":"Ghosh","sequence":"additional","affiliation":[{"name":"The Framingham Heart Study, Framingham, MA, USA"},{"name":"Boston University Chobanian & Avedisian School of Medicine"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9828-1776","authenticated-orcid":false,"given":"Jeremy","family":"Tanner","sequence":"additional","affiliation":[{"name":"Glenn Biggs Institute for Alzheimer's &amp; Neurodegenerative Diseases, University of Texas Health Sciences Center, San Antonio, TX, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Keith A.","family":"Johnson","sequence":"additional","affiliation":[{"name":"Department of Radiology, Massachusetts General Hospital, the Gordon Center for Medical Imaging and the Athinoula A. 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