{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,21]],"date-time":"2026-10-21T18:42:22Z","timestamp":1792608142107,"version":"4.5.0"},"reference-count":103,"publisher":"American Association for the Advancement of Science (AAAS)","issue":"809","content-domain":{"domain":["www.science.org"],"crossmark-restriction":true},"short-container-title":["Sci. Transl. Med."],"published-print":{"date-parts":[[2025,7,30]]},"abstract":"<jats:p>\n                    Cellular cross-talk, mediated by membrane receptors and their ligands, is crucial for brain homeostasis and can contribute to neurodegenerative diseases such as Alzheimer\u2019s disease (AD). To find cross-talk dysregulations involved in AD, we reconstructed cross-talk networks from single-nucleus transcriptional profiles of 67 clinically and neuropathologically well-characterized controls and AD brain donors from the Knight Alzheimer Disease Research Center and the Dominantly Inherited Alzheimer Network cohorts. We predicted a role for TREM2 and additional AD risk genes mediating neuron-microglia cross-talk in AD. We identified a gene network mediating neuron-microglia cross-talk through TREM2 and neuronal SEMA6D, which we predicted is disrupted in late AD stages. Using spatial transcriptomics on the human brain, we observed that the SEMA6D-TREM2 cross-talk gene network is activated near A\u03b2 plaques and SEMA6D-expressing cells. Using tissue immunostaining of human brains, we found that SEMA6D colocalizes with A\u03b2 plaques and TREM2-activated microglia. In addition, we found that plaque-proximal SEMA6D abundance decreased with the disease stage, which correlated with a reduction in microglial activation near plaques. These findings suggest that the loss of SEMA6D signaling impairs microglial activation and \u0391\u03b2 clearance. To validate this hypothesis, we leveraged\n                    <jats:italic toggle=\"yes\">TREM2<\/jats:italic>\n                    knockout human induced pluripotent stem cell\u2013derived microglia and observed that SEMA6D induces microglial activation and A\u03b2 plaque phagocytosis in a TREM2-dependent manner. In summary, we demonstrate that characterizing cellular cross-talk networks can yield insights into AD biology, provide additional context to understand AD genetic risk, and find previously unknown therapeutic targets and pathways.\n                  <\/jats:p>","DOI":"10.1126\/scitranslmed.adx0027","type":"journal-article","created":{"date-parts":[[2025,7,30]],"date-time":"2025-07-30T17:58:26Z","timestamp":1753898306000},"update-policy":"https:\/\/doi.org\/10.34133\/aaas_crossmark","source":"Crossref","is-referenced-by-count":16,"title":["Systematic analysis of cellular cross-talk reveals a role for SEMA6D-TREM2 regulating microglial function in Alzheimer\u2019s disease"],"prefix":"10.1126","volume":"17","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3651-0136","authenticated-orcid":true,"given":"Ricardo","family":"D\u2019Oliveira Albanus","sequence":"first","affiliation":[{"name":"Department of Psychiatry, Washington University School of Medicine, St. Louis, MO 63130, USA."},{"name":"Department of Neurology, Washington University School of Medicine, St. Louis, MO 63130, USA."},{"name":"Hope Center for Neurological Disorders, Washington University School of Medicine, St. Louis, MO 63130, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0003-1818-0150","authenticated-orcid":true,"given":"Gina M.","family":"Finan","sequence":"additional","affiliation":[{"name":"Department of Pathology and Cell Biology, Columbia University Irving Medical Center, New York, NY 10032, USA."},{"name":"Taub Institute for Research on Alzheimer\u2019s Disease and the Aging Brain, Columbia University Irving Medical Center, New York, NY 10032, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7175-3208","authenticated-orcid":true,"given":"Logan","family":"Brase","sequence":"additional","affiliation":[{"name":"Department of Psychiatry, Washington University School of Medicine, St. 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