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Here, we show that fragmented spatial exploration in APP\/PS1 mice correlates with diminished exploration\u2010evoked Ca\n                    <jats:sup>2+<\/jats:sup>\n                    transients in MEC layer II astrocytes. To address this, we transplanted glial progenitor cells into the MEC of aged AD mice. The engrafted cells differentiated into homeostatic astrocytes and restored perivascular Aquaporin\u20104 polarization. This remodeling significantly reduced amyloid\u2010beta burden, attenuated neuroinflammation, and preserved synaptic integrity. Crucially, these structural and molecular improvements specifically reversed spatial exploration deficits without affecting general locomotion. Together, our findings suggest that dysfunction in MECII astrocytes is associated with fragmented exploratory behavior. Furthermore, the region\u2010specific replacement of astrocytes may ameliorate the spatial exploration deficits observed in the AD mouse model.\n                  <\/jats:p>","DOI":"10.1002\/advs.77139","type":"journal-article","created":{"date-parts":[[2026,8,24]],"date-time":"2026-08-24T14:53:23Z","timestamp":1787583203000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Entorhinal Astrocyte Transplants Restore Spatial Exploration and Alleviate Amyloid\u2010Beta Pathology in Alzheimer's Mice"],"prefix":"10.1002","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-9936-4004","authenticated-orcid":false,"given":"Fengjuan","family":"Wu","sequence":"first","affiliation":[{"name":"Brain Research Center and State Key Laboratory of Trauma and Chemical Poisoning Third Military Medical University  Chongqing China"},{"name":"Department of Neurology Lanzhou University Second Hospital  Lanzhou 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