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We quantified expression of amyloid-\u03b2 (A\u03b2), pTau, and inflammatory and senescence markers across species. Distribution of AD-relevant markers were compared in FFPE and perfused frozen macaque brain to assess expression of labile proteins that could inform in-life fluid biomarkers.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>A\u03b2 pathology in macaques closely approximated patient pathology. Complex plaque composition in macaques implied significant disruption of synaptic connectivity. In FFPE tissue, pretangle pTau immunoreactivity placed the macaque in Braak Stage 1b. In perfused frozen tissue, soluble pTau distribution approximated Braak Stage III-IV. In macaque, A\u03b2, pTau, and acetylcholinesterase labeling co-localized to AD-vulnerable circuits. Significant association of glial fibrillary acidic protein with A\u03b2 occurred in humans only. The senescence marker p16 correlated positively with pTau expression and negatively with A\u03b2 in patients only. Macaques lacked neuropathologic co-morbidities.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>AD-relevant neuropathologic signals in the macaque support biomarker discovery in the areas of A\u03b2 plaque evolution and associated synaptic disruption as well as early-stage tau phosphorylation. Relative protection from accumulation of senescence markers, fibrillar tau and neuropathologic co-morbidities in macaque implicate species difference in rates of biological brain aging. We provide over 4000 digital slides for further study.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1177\/13872877251323787","type":"journal-article","created":{"date-parts":[[2025,3,17]],"date-time":"2025-03-17T12:36:11Z","timestamp":1742214971000},"page":"1243-1258","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":5,"title":["The neuropathologic basis for translational biomarker development in the macaque model of late-onset Alzheimer's disease"],"prefix":"10.1177","volume":"104","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1181-3544","authenticated-orcid":false,"given":"Caroline J","family":"Zeiss","sequence":"first","affiliation":[{"name":"Department of Comparative Medicine, Yale University School of Medicine, New Haven, CT, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2143-4329","authenticated-orcid":false,"given":"Anita","family":"Huttner","sequence":"additional","affiliation":[{"name":"Department of Pathology, Yale University School of Medicine, New Haven, CT, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7075-0195","authenticated-orcid":false,"given":"Angus C","family":"Nairn","sequence":"additional","affiliation":[{"name":"Department of Psychiatry, Yale University School of Medicine, New Haven, CT, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3420-1308","authenticated-orcid":false,"given":"Amy","family":"Arnsten","sequence":"additional","affiliation":[{"name":"Department of Neuroscience, Yale University School of Medicine, New Haven, CT, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5415-3067","authenticated-orcid":false,"given":"Dibyadeep","family":"Datta","sequence":"additional","affiliation":[{"name":"Department of Psychiatry, Yale University School of Medicine, New Haven, CT, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8188-3092","authenticated-orcid":false,"given":"Stephen M","family":"Strittmatter","sequence":"additional","affiliation":[{"name":"Department of Neuroscience, Yale University School of Medicine, New Haven, CT, USA"},{"name":"Department of Neurology, Yale University School of Medicine, New Haven, CT, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3990-3955","authenticated-orcid":false,"given":"Brent Vander","family":"Wyk","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Yale University School of Medicine, New Haven, CT, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5086-5438","authenticated-orcid":false,"given":"Alvaro","family":"Duque","sequence":"additional","affiliation":[{"name":"Department of Neuroscience, Yale University School of Medicine, New Haven, CT, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","published-online":{"date-parts":[[2025,3,17]]},"reference":[{"key":"e_1_3_5_2_2","doi-asserted-by":"publisher","DOI":"10.3389\/fnagi.2021.734173"},{"key":"e_1_3_5_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/0197-4580(93)90067-L"},{"key":"e_1_3_5_4_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.jalz.2017.11.005"},{"key":"e_1_3_5_5_2","doi-asserted-by":"publisher","DOI":"10.1002\/ajp.23299"},{"key":"e_1_3_5_6_2","article-title":"Bridging the rodent to human translational gap: marmosets as model systems for the study of Alzheimer's disease","volume":"9","author":"Sukoff Rizzo SJ","year":"2023","unstructured":"Sukoff Rizzo SJ, Homanics G, Schaeffer DJ, et al. 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