{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,19]],"date-time":"2026-10-19T15:53:15Z","timestamp":1792425195581,"version":"4.5.0"},"reference-count":55,"publisher":"American Association for the Advancement of Science (AAAS)","issue":"22","content-domain":{"domain":["www.science.org"],"crossmark-restriction":true},"short-container-title":["Sci. Adv."],"published-print":{"date-parts":[[2024,5,31]]},"abstract":"<jats:p>\n            Immunosenescence contributes to systematic aging and plays a role in the pathogenesis of Alzheimer\u2019s disease (AD). Therefore, the objective of this study was to investigate the potential of immune rejuvenation as a therapeutic strategy for AD. To achieve this, the immune systems of aged\n            <jats:italic>APP\/PS1<\/jats:italic>\n            mice were rejuvenated through young bone marrow transplantation (BMT). Single-cell RNA sequencing revealed that young BMT restored the expression of aging- and AD-related genes in multiple cell types within blood immune cells. The level of circulating senescence-associated secretory phenotype proteins was decreased following young BMT. Notably, young BMT resulted in a significant reduction in cerebral A\u03b2 plaque burden, neuronal degeneration, neuroinflammation, and improvement of behavioral deficits in aged\n            <jats:italic>APP\/PS1<\/jats:italic>\n            mice. The ameliorated cerebral amyloidosis was associated with an enhanced A\u03b2 clearance of peripheral monocytes. In conclusion, our study provides evidence that immune system rejuvenation represents a promising therapeutic approach for AD.\n          <\/jats:p>","DOI":"10.1126\/sciadv.adl1123","type":"journal-article","created":{"date-parts":[[2024,5,29]],"date-time":"2024-05-29T17:58:57Z","timestamp":1717005537000},"update-policy":"https:\/\/doi.org\/10.34133\/aaas_crossmark","source":"Crossref","is-referenced-by-count":49,"title":["Rejuvenation of peripheral immune cells attenuates Alzheimer\u2019s disease-like pathologies and behavioral deficits in a mouse model"],"prefix":"10.1126","volume":"10","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-2330-873X","authenticated-orcid":true,"given":"Pu-Yang","family":"Sun","sequence":"first","affiliation":[{"name":"Department of Neurology, Daping Hospital, Third Military Medical University, Chongqing, China."},{"name":"Chongqing Key Laboratory of Aging and Brain Diseases, Chongqing, 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