{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,20]],"date-time":"2026-08-20T02:25:28Z","timestamp":1787192728495,"version":"build-2736575974"},"reference-count":26,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2026,8,6]],"date-time":"2026-08-06T00:00:00Z","timestamp":1785974400000},"content-version":"vor","delay-in-days":5,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2026,8,1]],"date-time":"2026-08-01T00:00:00Z","timestamp":1785542400000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Intl J of Devlp Neuroscience"],"published-print":{"date-parts":[[2026,8]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Alzheimer's disease (\n                    <jats:sc>AD<\/jats:sc>\n                    ) represents the most prevalent neurodegenerative disorder worldwide, affecting millions of individuals and imposing substantial socioeconomic burdens. While traditional research has focused on amyloid\u2010\u03b2 (A\u03b2) plaques and neurofibrillary tangles as primary pathological hallmarks, mounting evidence implicates neuroinflammation as a critical third pillar in\n                    <jats:sc>AD<\/jats:sc>\n                    pathogenesis. This review critically evaluates current understanding of neuroinflammatory mechanisms in\n                    <jats:sc>AD<\/jats:sc>\n                    , examining the complex interplay between cellular mediators, molecular pathways and environmental triggers across a temporal disease\u2010stage framework. We explore the dual and stage\u2010dependent roles of microglia and astrocytes, expand discussion of blood\u2013brain barrier (BBB) dysfunction and peripheral immune infiltration as underappreciated pathogenic contributors, and integrate emerging evidence linking neuroinflammation specifically to tau pathology and its stereotyped propagation through the brain. Diagnostic biomarkers, including translocator protein\u2013positron emission tomography (TSPO\u2010PET) and plasma glial fibrillary acidic protein (GFAP), are evaluated with explicit attention to clinical utility, technical limitations, and their relationship to established\n                    <jats:sc>AD<\/jats:sc>\n                    biomarkers. Therapeutic strategies are critically assessed with careful distinction between preclinical proof\u2010of\u2010concept data and available clinical evidence, and key translational challenges are highlighted throughout. The review emphasizes the need for stage\u2010appropriate intervention windows, patient stratification by neuroinflammatory endotype, and biologically rational combination strategies. Understanding neuroinflammation's temporal and spatial dynamics offers promising but as yet insufficiently realized avenues for early intervention and disease modification in\n                    <jats:sc>AD<\/jats:sc>\n                    .\n                  <\/jats:p>","DOI":"10.1002\/jdn.70168","type":"journal-article","created":{"date-parts":[[2026,8,6]],"date-time":"2026-08-06T13:22:42Z","timestamp":1786022562000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Mechanisms, Biomarkers and Therapeutic Implications of Neuroinflammation in Alzheimer's Disease"],"prefix":"10.1002","volume":"86","author":[{"ORCID":"https:\/\/orcid.org\/0009-0004-2833-9599","authenticated-orcid":false,"given":"Shaunt","family":"Papelian","sequence":"first","affiliation":[{"name":"Department of Cell Biology and Neuroscience University of California  Riverside California 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