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This review examines how chemokine systems transition from tightly regulated homeostatic signals to drivers of chronic neuroinflammation in AD. We describe the major chemokine families (CC, CXC, CX3C) and their dominant central nervous system (CNS) receptors (CCR2, CXCR3, CX3CR1), which activate canonical inflammatory pathways including NF\u2010\u03baB, JAK\/STAT and PI3K\u2010AKT. In AD, chemokine dysregulation occurs in a coordinated manner across multiple functional modules, including recruitment\u2010associated (CCL2, CXCL1), interferon\u2010inducible (CXCL10), loss\u2010of\u2010restraint (CX3CL1) and vascular\u2010associated chemokines. These alterations shift the network from regulated immune communication to self\u2010sustaining inflammatory circuits perpetuating chronic neuroinflammation. These networks reprogram microglia and astrocytes into disease\u2010associated phenotypes, amplify peripheral immune cell infiltration and destabilise synaptic function. Biological sex profoundly influences neuroinflammatory trajectories, with females exhibiting enhanced microglial senescence and interferon signalling, while males show accelerated complement activation. Viral pathogens, particularly neurotropic viruses (HSV\u20101, HHV\u20106, VZV) and SARS\u2010CoV\u20102, actively reprogram chemokine networks, linking infection to amyloid\u2010\u03b2 accumulation, tau pathology and neurodegeneration. Therapeutically, chemokine axes represent precision targets requiring stage\u2010matched, sex\u2010stratified interventions rather than broad anti\u2010inflammatory approaches. Understanding chemokine network dynamics offers mechanistic insights into AD pathogenesis and could provide pointers for therapeutic strategies.<\/jats:p>","DOI":"10.1111\/bcpt.70273","type":"journal-article","created":{"date-parts":[[2026,7,8]],"date-time":"2026-07-08T04:13:46Z","timestamp":1783484026000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Chemokines in Alzheimer's Disease: Early Defence, Late Damage and the Impact of Sex and Infection"],"prefix":"10.1111","volume":"139","author":[{"given":"Blanca I.","family":"Aldana","sequence":"first","affiliation":[{"name":"Department of Veterinary and Animal Sciences, Faculty of Health and Medical Sciences University of Copenhagen  Frederiksberg Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kristine","family":"Freude","sequence":"additional","affiliation":[{"name":"Department of Veterinary and Animal Sciences, Faculty of Health and 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