{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,17]],"date-time":"2026-09-17T23:54:34Z","timestamp":1789689274666,"version":"4.0.1"},"reference-count":33,"publisher":"SAGE Publications","issue":"3","license":[{"start":{"date-parts":[[2026,6,18]],"date-time":"2026-06-18T00:00:00Z","timestamp":1781740800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"funder":[{"DOI":"10.13039\/100000957","name":"Alzheimer's Association","doi-asserted-by":"publisher","award":["25AARG-1378979"],"award-info":[{"award-number":["25AARG-1378979"]}],"id":[{"id":"10.13039\/100000957","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100007625","name":"Cure Alzheimer's Fund","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100007625","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000049","name":"National Institute on Aging","doi-asserted-by":"publisher","award":["R01AG082185"],"award-info":[{"award-number":["R01AG082185"]}],"id":[{"id":"10.13039\/100000049","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000050","name":"National Heart, Lung, and Blood Institute","doi-asserted-by":"publisher","award":["R01HL158534"],"award-info":[{"award-number":["R01HL158534"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000050","name":"National Heart, Lung, and Blood Institute","doi-asserted-by":"publisher","award":["R01HL178835"],"award-info":[{"award-number":["R01HL178835"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Journal of Alzheimer\u2019s Disease"],"published-print":{"date-parts":[[2026,8]]},"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Clonal hematopoiesis (CH) increases with age and elevates the risk of numerous age-associated diseases. However, the association between CH and neurodegenerative diseases has remained unclear.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>We tested the association between the presence of CH and tauopathy in a murine model.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      We established novel models of\n                      <jats:italic toggle=\"yes\">Tet2<\/jats:italic>\n                      loss-of-function and\n                      <jats:italic toggle=\"yes\">Jak2<\/jats:italic>\n                      gain-of-function (V617F) CH in CD45.1-expressing\n                      <jats:italic toggle=\"yes\">PS19<\/jats:italic>\n                      tauopathy mice using unconditioned bone marrow (BM) cell transfer, thereby maintaining brain integrity, clonal expansion, and enabling mutant cell tracking.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      In CD45.1-\n                      <jats:italic toggle=\"yes\">PS19<\/jats:italic>\n                      mice,\n                      <jats:italic toggle=\"yes\">\n                        Tet2\n                        <jats:sup>-\/-<\/jats:sup>\n                      <\/jats:italic>\n                      cells (CD45.2) started at a fraction of &lt;2% and clonally expanded in all BM cavities and the blood over 5 months.\n                      <jats:italic toggle=\"yes\">Tet2<\/jats:italic>\n                      mutant and WT immune cells, however, displayed equivalently low capacity to infiltrate the brain of\n                      <jats:italic toggle=\"yes\">PS19<\/jats:italic>\n                      mice even with advanced tau deposition. While\n                      <jats:italic toggle=\"yes\">Tet2<\/jats:italic>\n                      mutant microglia displayed elevated IL1-\u03b2 production, they comprised a small fraction (3.49\u2009\u00b1\u20091.35%) relative to the high frequency of mutant monocytes in the blood (26.36\u2009\u00b1\u20094.33%) of aged CD45.1-\n                      <jats:italic toggle=\"yes\">PS19<\/jats:italic>\n                      mice after clonal expansion.\n                      <jats:italic toggle=\"yes\">\n                        Jak2\n                        <jats:sup>V617F<\/jats:sup>\n                      <\/jats:italic>\n                      cells (CD45.2) also expanded clonally in the BM and blood over time and had a modestly increased capacity to infiltrate the brain of aged CD45.1-\n                      <jats:italic toggle=\"yes\">PS19<\/jats:italic>\n                      mice but their proportion among brain microglia remained low (1.12\u2009\u00b1\u20090.28%) relative to blood monocytes (28.91\u2009\u00b1\u20094.66%). Critically,\n                      <jats:italic toggle=\"yes\">Tet2<\/jats:italic>\n                      or\n                      <jats:italic toggle=\"yes\">Jak2<\/jats:italic>\n                      CH did not alter tau accumulation in the hippocampus or cortex, nor did they influence brain atrophy.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Our findings suggest that CH mutant cells do not influx the murine tauopathy brain in large proportions and that CH does not modify neurodegeneration or tau accumulation in mice.<\/jats:p>\n                  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