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In addition to neurons, astrocytes modulate neuronal network activity through tripartite synapses. Also, astrocytes are increasingly recognized for their involvement in AD pathology. Aberrant astrocytic calcium signaling has been implicated in AD pathological processes, including disrupted synaptic transmission, dysregulated glutamate homeostasis, and impaired vascular function via astrocytic endfeet. Previous investigations have assessed compartment-specific astrocytic calcium transients, yet most employed a restricted range of metrics. Thus, comprehensive analyses of calcium dynamics within individual astrocytic compartments in mouse models of amyloidosis are lacking.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>To analyze spontaneous calcium transients within distinct astrocytic compartments in APP\/PS1 mice.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Using in vivo multiphoton imaging of Yellow Cameleon 3.6, a genetically encoded calcium indicator targeted to astrocytes in APP\/PS1 mice, we analyzed spontaneous calcium transients in cortical astrocytes at 4\u20136 months of age. We quantified event rate, activity duration, area under the curve (AUC), and peak amplitude across four compartments: soma, processes, microdomains, and endfeet. Correlation analyses were used to assess astrocyte synchrony and distance-dependent activity relationships.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>In APP\/PS1 mice, somas exhibited increased activity duration and peak amplitude, while processes and microdomains showed reduced duration, AUC, and amplitude despite higher event rates. Endfeet showed reductions in all parameters. Correlation analyses revealed enhanced astrocyte synchrony in APP\/PS1 mice, with distance-dependent correlation decay observed only in nontransgenic controls.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>These findings highlight compartment-specific disruptions of astrocytic calcium activity caused by amyloidosis.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1177\/13872877261464208","type":"journal-article","created":{"date-parts":[[2026,6,30]],"date-time":"2026-06-30T18:07:32Z","timestamp":1782842852000},"page":"2007-2021","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":0,"title":["Compartment-specific analysis reveals disrupted astrocytic calcium transients in anesthetized Alzheimer's disease mice"],"prefix":"10.1177","volume":"112","author":[{"ORCID":"https:\/\/orcid.org\/0009-0008-1827-7426","authenticated-orcid":false,"given":"Md Joynal","family":"Abedin","sequence":"first","affiliation":[{"name":"Department of Neurology, Mass General Brigham, Harvard Medical School, Charlestown, MA, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yee Fun","family":"Lee","sequence":"additional","affiliation":[{"name":"Department of Neurology, Mass General Brigham, Harvard Medical School, Charlestown, MA, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Melinda","family":"Zhang","sequence":"additional","affiliation":[{"name":"Brown University"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alyssa N","family":"Russ","sequence":"additional","affiliation":[{"name":"Department of Neurology, Mass General Brigham, Harvard Medical School, Charlestown, MA, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dmitry","family":"Gerashchenko","sequence":"additional","affiliation":[{"name":"Department of Psychiatry, Harvard Medical School and Veterans Affairs Boston Healthcare System, West Roxbury, MA, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Brian J.","family":"Bacskai","sequence":"additional","affiliation":[{"name":"Department of Neurology, Mass General Brigham, Harvard Medical School, Charlestown, MA, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3727-0317","authenticated-orcid":false,"given":"Ksenia V.","family":"Kastanenka","sequence":"additional","affiliation":[{"name":"Department of Neurology, Mass General Brigham, Harvard Medical School, Charlestown, MA, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","published-online":{"date-parts":[[2026,6,30]]},"reference":[{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1001\/jama.2019.4782"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.31887\/DCNS.2013.15.4\/hjahn"},{"key":"e_1_3_3_4_2","doi-asserted-by":"publisher","DOI":"10.1111\/ene.13439"},{"key":"e_1_3_3_5_2","doi-asserted-by":"publisher","DOI":"10.15252\/emmm.201606210"},{"key":"e_1_3_3_6_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.jalz.2011.10.007"},{"key":"e_1_3_3_7_2","doi-asserted-by":"publisher","DOI":"10.1016\/bs.irn.2020.01.006"},{"key":"e_1_3_3_8_2","doi-asserted-by":"publisher","DOI":"10.1038\/nn.2583"},{"key":"e_1_3_3_9_2","first-page":"153","article-title":"Network excitability dysfunction in Alzheimer\u2019s disease: insights from in vitro and in vivo models","volume":"21","author":"Santos SF","year":"2010","unstructured":"Santos SF, Pierrot N, Octave J-N. 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