{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,4]],"date-time":"2026-08-04T05:47:41Z","timestamp":1785822461092,"version":"3.56.0"},"reference-count":240,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,8,4]],"date-time":"2026-08-04T00:00:00Z","timestamp":1785801600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Aging Neurosci."],"abstract":"<jats:p>Alzheimer\u2019s disease (AD) has long been framed around amyloid-beta (A\u03b2) and tau pathology, yet mounting evidence indicates that dysfunctional microglia\u2013astrocyte crosstalk is an important, and often underappreciated, contributor to disease progression that operates alongside\u2014rather than in place of\u2014neuronal, vascular, and proteinopathic mechanisms. Here we propose a three-stage framework in which glial communication transitions from silent vulnerability through organized defense to maladaptive collapse. During preclinical aging, gut dysbiosis, diminished tryptophan-derived aryl hydrocarbon receptor (AHR) ligands, and blood\u2013brain barrier weakening prime glia toward inflammatory states with elevated complement tone. Upon A\u03b2 accumulation, microglia and astrocytes initially mount a compensatory response\u2014forming reactive glial nets, containing plaques, clearing tau, and executing complement-guided synaptic pruning. However, sustained pathological burden triggers self-reinforcing loops involving the C3\u2013C3aR axis and IL-1\u03b1\/TNF-\u03b1\/C1q signaling, converting the glial network into a propagation engine for tau spreading and synapse loss\u2014the strongest correlate of cognitive decline. We discuss the tryptophan\u2013microbiota\u2013AHR axis as one candidate upstream modulator, while emphasizing that direct human evidence remains limited, and highlight APOE4 in exacerbating microglia-dependent synaptic phagocytosis. To support testability, we operationally define maladaptive loops and communication collapse, and specify measurable variables, fluid\/imaging biomarker proxies (e.g., the sTREM2\/GFAP ratio), and falsifiable predictions. This framework, presented as an integrative hypothesis rather than an established principle, argues that future therapies must combine protein-targeted approaches with restoration of glial communication homeostasis.<\/jats:p>","DOI":"10.3389\/fnagi.2026.1908574","type":"journal-article","created":{"date-parts":[[2026,8,4]],"date-time":"2026-08-04T05:39:27Z","timestamp":1785821967000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Microglia\u2013astrocyte crosstalk as a key organizing principle of Alzheimer\u2019s disease: from homeostatic cooperation to maladaptive signaling loops"],"prefix":"10.3389","volume":"18","author":[{"given":"Mingqiang","family":"Gong","sequence":"first","affiliation":[{"name":"Shenzhen Bao\u2019an Chinese Medicine Hospital, Guangzhou University of Chinese Medicine, Shenzhen","place":["Guangdong, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jiao","family":"Lan","sequence":"additional","affiliation":[{"name":"Shenzhen Bao\u2019an Chinese Medicine Hospital, Guangzhou University of Chinese Medicine, Shenzhen","place":["Guangdong, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jifei","family":"Miao","sequence":"additional","affiliation":[{"name":"Shenzhen Bao\u2019an Chinese Medicine Hospital, Guangzhou University of Chinese Medicine, Shenzhen","place":["Guangdong, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2026,8,4]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"41","DOI":"10.1038\/nrn1824","article-title":"Astrocyte-endothelial interactions at the blood-brain barrier.","volume":"7","author":"Abbott","year":"2006","journal-title":"Nat. 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