{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"institution":[{"name":"bioRxiv"}],"indexed":{"date-parts":[[2026,2,16]],"date-time":"2026-02-16T17:33:43Z","timestamp":1771263223103,"version":"3.50.1"},"posted":{"date-parts":[[2025,10,19]]},"group-title":"Neuroscience","reference-count":138,"publisher":"openRxiv","license":[{"start":{"date-parts":[[2025,10,19]],"date-time":"2025-10-19T00:00:00Z","timestamp":1760832000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/www.biorxiv.org\/about\/FAQ#license"}],"funder":[{"name":"NIH\/NIA","award":["R01AG091577"],"award-info":[{"award-number":["R01AG091577"]}]},{"name":"Strang Neuroscience Research Award"},{"name":"Virginia Alzheimer\u2019s disease Center"},{"name":"UVA Brain Institute Transformative Neuroscience Pilot Grant"},{"name":"Commonwealth Health Research Board Award"},{"DOI":"10.13039\/100007625","name":"Cure Alzheimer's Fund","doi-asserted-by":"crossref","id":[{"id":"10.13039\/100007625","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"accepted":{"date-parts":[[2025,10,19]]},"abstract":"<jats:title>SUMMARY<\/jats:title>\n                <jats:p>Alzheimer\u2019s disease (AD) research has been hindered by the lack of models that faithfully recapitulate the full profile of disease progression in a human genetic background. We developed a 3D assembloid model (\u201cMasteroid\u201d) using iPSC-derived neurons, astrocytes, and microglia from APOE4\/4 and isogenic control lines. Neurons were seeded with tau oligomers, then combined with astrocytes and microglia to form mature 3D Masteroids, followed by amyloid-\u03b2 oligomer exposure. After four weeks, AD-Masteroids exhibited hallmark pathologies, including extracellular amyloid-\u03b2 deposits, intracellular tau aggregation, neurodegeneration, astrogliosis, and microglial activation, with APOE4 exacerbating all phenotypes. Single-cell RNA sequencing further identified novel roles of IGFBP pathways in amyloid-\u03b2 and tau-mediated pathology. This innovative platform provides a robust system to dissect cellular and molecular mechanisms of AD progression and offers a powerful tool for therapeutic discovery.<\/jats:p>\n                <jats:sec>\n                  <jats:title>Highlights<\/jats:title>\n                  <jats:list list-type=\"bullet\">\n                    <jats:list-item>\n                      <jats:p>The 3D human neuron\u2013glia assembloid (\u201cMasteroid\u201d), composed of neurons, astrocytes, microglia, and oligodendrocytes, faithfully recapitulates human brain ultrastructure and intercellular interactions.<\/jats:p>\n                    <\/jats:list-item>\n                    <jats:list-item>\n                      <jats:p>Exposure to oligomeric tau and A\u03b2 induced hallmark Alzheimer\u2019s pathologies, including amyloid deposition, tau aggregation, neurodegeneration, and gliosis.<\/jats:p>\n                    <\/jats:list-item>\n                    <jats:list-item>\n                      <jats:p>The APOE4 genotype exacerbated all pathological features, highlighting its role in driving multicellular interactions that accelerate disease progression.<\/jats:p>\n                    <\/jats:list-item>\n                    <jats:list-item>\n                      <jats:p>The IGF signaling axis was identified as a key mediator of A\u03b2- and tau-induced pathology and a potential therapeutic target.<\/jats:p>\n                    <\/jats:list-item>\n                  <\/jats:list>\n                <\/jats:sec>\n                <jats:sec>\n                  <jats:title>Graphical Abstract<\/jats:title>\n                  <jats:fig id=\"ufig1\" position=\"float\" orientation=\"portrait\" fig-type=\"figure\">\n                    <jats:graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"683162v1_ufig1\" position=\"float\" orientation=\"portrait\"\/>\n                  <\/jats:fig>\n                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