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Synaptic plasticity and neuroinflammation are hallmarks of\n                    <jats:sc>AD<\/jats:sc>\n                    , with their dysregulation forming a self\u2010reinforcing cycle that aggravates neurodegeneration. Proinflammatory cytokines impair synaptic signaling by suppressing brain\u2010derived neurotrophic factor (BDNF) expression and neuroplasticity markers, further compromising synaptic plasticity. \u03b2\u2010Caryophyllene (BCP), a natural bicyclic sesquiterpene with anti\u2010inflammatory and neuroprotective properties, may counteract these pathological processes. This study evaluated the effect of BCP in mitigating streptozotocin (STZ)\u2010induced\n                    <jats:sc>AD<\/jats:sc>\n                    \u2010like conditions in male Sprague\u2013Dawley rats. Two doses of STZ (3\u2009mg\/kg) on Days 1 and 3 were administered intracerebroventricularly to induce\n                    <jats:sc>AD<\/jats:sc>\n                    \u2010like pathology. Rats received BCP (10, 20\u2009mg\/kg, i.p.) or rivastigmine (2.5\u2009mg\/kg) for 28\u2009days. Cognitive performance was assessed using the Barnes maze and novel object recognition tests. Hippocampal tissues were analyzed for BDNF expression, synaptic plasticity markers (e.g., synaptophysin, neural cell adhesion molecule [NCAM], and ciliary neurotrophic factor [CNTF]), neuroinflammatory markers (e.g., IL\u20101\u03b2, TNF\u2010\u03b1, IL\u20106, COX2, and NF\u2010\u03baB), and oxidative stress markers. Histological (hematoxylin and eosin) and Golgi\u2010Cox staining techniques were employed to evaluate neuronal integrity and synaptic organization. STZ\u2010induced rats exhibited significant cognitive deficits, synaptic loss, and increased neuroinflammation. BCP treatment improved spatial learning and memory retention, increased BDNF expression, and restored synaptic plasticity markers. Furthermore, BCP attenuated neuroinflammation by reducing proinflammatory cytokine levels. Histopathology confirms normal hippocampal neuronal architecture in BCP\u2010treated groups. These findings highlight the ability of BCP to modulate BDNF signaling, synaptic plasticity, and neuroinflammatory pathways, underscoring its potential as a multitarget therapeutic candidate for\n                    <jats:sc>AD<\/jats:sc>\n                    .\n                  <\/jats:p>","DOI":"10.1111\/ejn.70317","type":"journal-article","created":{"date-parts":[[2025,11,19]],"date-time":"2025-11-19T05:11:08Z","timestamp":1763529068000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["\u03b2\u2010Caryophyllene Ameliorates STZ\u2010Induced Alzheimer's Disease\u2010Like Conditions in Rats via Modulation of Brain\u2010Derived Neurotrophic Factor, Synaptic Plasticity, and Neuroinflammation"],"prefix":"10.1111","volume":"62","author":[{"given":"Sumit\u00a0S.","family":"Rathod","sequence":"first","affiliation":[{"name":"R.C. Patel Institute of Pharmaceutical Education and Research  Shirpur Maharashtra India"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1402-548X","authenticated-orcid":false,"given":"Yogeeta\u00a0O.","family":"Agrawal","sequence":"additional","affiliation":[{"name":"R.C. 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