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Amyloid-\u03b2 (A\u03b2) and tau aggregation, mitochondrial dysfunction, and microglial dysregulation are key contributors to AD pathogenesis. Impairments in the blood-brain barrier have unveiled the contribution of the immune system, particularly B cells, in AD pathology. B cells, a crucial component of adaptive immunity, exhibit diverse functions, including antigen presentation and antibody production. While their role in neuroinflammatory disorders has been well-documented, their specific function in AD lacks adequate data. This review examines the dual role of the B cells and humoral immunity in modulating brain inflammation in AD and explores recent advancements in passive and active immunotherapeutic strategies targeting AD pathobiology. We summarize preclinical and clinical studies investigating B cell frequency, altered antibody levels, and their implications in neuroinflammation and immunotherapy. Notably, B cells demonstrate protective and pathological roles in AD, influencing neurodegeneration through antibody-mediated clearance of toxic aggregates and inflammatory activation inflammation. Passive immunotherapies targeting A\u03b2 have shown potential in reducing amyloid plaques, while active immunotherapies are emerging as promising strategies, requiring further validation. Understanding the interplay between B cells, humoral immunity, microglia, and mitochondrial dysfunction is critical to unraveling AD pathogenesis. Their dual nature in disease progression underscores the need for precise therapeutic interventions to optimize immunotherapy outcomes and mitigate neuroinflammation effectively.<\/jats:p>","DOI":"10.1177\/25424823251329188","type":"journal-article","created":{"date-parts":[[2025,4,28]],"date-time":"2025-04-28T01:09:27Z","timestamp":1745802567000},"update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":10,"title":["Alzheimer's disease and the immune system: A comprehensive overview with a focus on B cells, humoral immunity, and immunotherapy"],"prefix":"10.1177","volume":"9","author":[{"given":"Ladan","family":"Gol Mohammad Pour Afrakoti","sequence":"first","affiliation":[{"name":"Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sanam","family":"Daneshpour Moghadam","sequence":"additional","affiliation":[{"name":"Department of Diagnostic and Public Health, School of Biotechnology, University of Verona, Verona, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8746-198X","authenticated-orcid":false,"given":"Pezhman","family":"Hadinezhad","sequence":"additional","affiliation":[{"name":"Cognitive Neurology, Dementia and Neuropsychiatry Research Center, Tehran University of Medical Sciences, Tehran, Iran"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","published-online":{"date-parts":[[2025,4,27]]},"reference":[{"key":"e_1_3_4_2_2","doi-asserted-by":"publisher","DOI":"10.1002\/ca.980080612"},{"key":"e_1_3_4_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.arcmed.2007.10.001"},{"key":"e_1_3_4_4_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.immuni.2022.10.016"},{"key":"e_1_3_4_5_2","doi-asserted-by":"publisher","DOI":"10.1093\/brain\/awy151"},{"key":"e_1_3_4_6_2","doi-asserted-by":"publisher","DOI":"10.1007\/s00415-013-7145-2"},{"key":"e_1_3_4_7_2","doi-asserted-by":"publisher","DOI":"10.1002\/cyto.b.20542"},{"key":"e_1_3_4_8_2","doi-asserted-by":"publisher","DOI":"10.3390\/cells10071605"},{"key":"e_1_3_4_9_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.brainresrev.2004.09.009"},{"key":"e_1_3_4_10_2","article-title":"Cognitive symptoms of Alzheimer\u2019s disease: clinical management and prevention","volume":"367","author":"Joe E","year":"2019","unstructured":"Joe E, Ringman JM. 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