{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,24]],"date-time":"2026-08-24T12:25:03Z","timestamp":1787574303832,"version":"build-2736575974"},"reference-count":78,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,8,24]],"date-time":"2026-08-24T00:00:00Z","timestamp":1787529600000},"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. Mol. Neurosci."],"abstract":"<jats:p>Women are twice as likely to develop Alzheimer\u2019s disease (AD) as men. Despite substantial progress in understanding the pathogenesis of sporadic AD, sex-specific mechanisms remain insufficiently explored, and preclinical research has historically been biased toward male subjects. Furthermore, there is often a delay of more than 10 years between the onset of neuropathological changes and clinical diagnosis. This latent pre-symptomatic period, during which pathological alterations may still be reversible, represents a promising window for therapeutic intervention. In this context, synaptic dysfunction and neuroinflammatory alterations are among the earliest detectable AD-associated impairments and have recently emerged as promising therapeutic targets. This mini-review summarizes the currently limited knowledge on sex-related differences in synaptic functions during pre-symptomatic stage of AD pathology in both pre-clinical and clinical studies. We further position sex as a critical biological variable impacting neuronal activity, either directly or indirectly through microglia-neuron crosstalk. Finally, we emphasize the importance and rationale for integrating sex-specific neuroimmune mechanisms into early-stage research to guide design of targeted, sex-tailored therapeutic strategies that modulate neuron-microglia interactions before clinical onset.<\/jats:p>","DOI":"10.3389\/fnmol.2026.1905780","type":"journal-article","created":{"date-parts":[[2026,8,24]],"date-time":"2026-08-24T11:50:56Z","timestamp":1787572256000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Update on sex-specific microglia contribution to early synaptic dysfunction in Alzheimer\u2019s disease"],"prefix":"10.3389","volume":"19","author":[{"given":"Candice M.","family":"Roux","sequence":"first","affiliation":[{"name":"Department of Cell and Developmental Biology, Division of Biosciences, University College London","place":["London, UK"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Slavica","family":"Krantic","sequence":"additional","affiliation":[{"name":"Neuroimmunology, Inflammation and Therapeutics Laboratory, Inserm U938, Centre De Recherche Saint-Antoine (CRSA), Sorbonne Universit\u00e9","place":["Paris, France"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2026,8,24]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"264","DOI":"10.1016\/j.ceca.2009.12.010","article-title":"Amyloid \u03b2 oligomers induce Ca2+ dysregulation and neuronal death through activation of ionotropic glutamate receptors.","volume":"47","author":"Alberdi","year":"2010","journal-title":"Cell Calcium"},{"key":"B2","doi-asserted-by":"publisher","first-page":"867","DOI":"10.1111\/j.1528-1167.2006.00554.x","article-title":"Incidence and predictors of seizures in patients with Alzheimer\u2019s disease.","volume":"47","author":"Amatniek","year":"2006","journal-title":"Epilepsia"},{"key":"B3","doi-asserted-by":"publisher","first-page":"37","DOI":"10.3390\/neurolint18020037","article-title":"Alzheimer\u2019s disease as a disorder of neuroimmune dysregulation.","volume":"18","author":"Aranda-Abreu","year":"2026","journal-title":"Neurol. 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