{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,24]],"date-time":"2026-10-24T00:12:50Z","timestamp":1792800770780,"version":"4.5.0"},"reference-count":303,"publisher":"SAGE Publications","license":[{"start":{"date-parts":[[2026,2,1]],"date-time":"2026-02-01T00:00:00Z","timestamp":1769904000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"},{"start":{"date-parts":[[2026,2,1]],"date-time":"2026-02-01T00:00:00Z","timestamp":1769904000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Journal of Alzheimer's Disease Reports"],"published-print":{"date-parts":[[2026,2]]},"abstract":"<jats:p>\n                    This narrative review aims to synthesize and critically evaluate the complex molecular mechanisms by which amyloid-\u03b2 (A\u03b2) accumulation disrupts hippocampal synaptic plasticity, the cellular cornerstone of learning and memory in Alzheimer's disease (AD). AD is characterized by progressive hippocampus-dependent cognitive decline, strongly linked to impaired synaptic plasticity, the cellular basis of learning and memory. This review deciphers how A\u03b2 accumulation orchestrates synaptic sabotage in the hippocampus. We detail the core molecular machinery of hippocampal synaptic plasticity, emphasizing glutamate receptor trafficking (NMDAR\/AMPAR), Ca\n                    <jats:sup>2+<\/jats:sup>\n                    signaling, and neurotrophin pathways (BDNF\/TrkB). Central to AD pathogenesis, soluble A\u03b2 oligomers initiate synaptic dysfunction by targeting receptors like PrP\u1d9c\/mGluR5, triggering NMDAR overactivation (via Fyn\/NR2B) and AMPAR endocytosis. A\u03b2 further drives tau hyperphosphorylation (via GSK-3\u03b2\/CDK5), leading to dendritic p-tau accumulation and destabilization of the postsynaptic density (PSD). Concurrently, A\u03b2 activates microglia (via TLR4\/TREM2) and astrocytes, promoting neuroinflammation (IL-1\u03b2, TNF-\u03b1, C1q) and complement-mediated synaptic phagocytosis. A\u03b2-induced oxidative stress (ROS\/RNS, lipid peroxidation) and mitochondrial failure (mPTP opening, energy depletion) exacerbate Ca\n                    <jats:sup>2+<\/jats:sup>\n                    dyshomeostasis and plasticity impairment. Critically, A\u03b2 disrupts BDNF\/TrkB signaling, promoting proBDNF\/p75\u1d3a\u1d40\u1d3f-mediated spine loss and inhibiting CREB-dependent plasticity gene expression. These converging pathways\u2014glutamate receptor dysregulation, p-tau toxicity, neuroinflammation, oxidative stress, mitochondrial dysfunction, and neurotrophic collapse\u2014culminate in synaptic apoptosis, profound structural damage (spine loss, PSD dissolution), and functional deficits (long-term potentiation (LTP) blockade, enhanced long-term depression (LTD)). This molecular cascade directly underlies hippocampal circuit failure and cognitive decline in AD. Future research must address A\u03b2 strain specificity, regional vulnerability, glial metabolic coupling, resilience mechanisms, and novel therapeutic strategies targeting these pathways.\n                  <\/jats:p>","DOI":"10.1177\/25424823261415807","type":"journal-article","created":{"date-parts":[[2026,2,6]],"date-time":"2026-02-06T17:38:54Z","timestamp":1770399534000},"update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":10,"title":["Molecular sabotage of hippocampal synaptic plasticity by amyloid-\u03b2 in Alzheimer's disease: A narrative review"],"prefix":"10.1177","volume":"10","author":[{"given":"Zahra","family":"Behroozi","sequence":"first","affiliation":[{"name":"Jiroft University of Medical Sciences"},{"name":"Jiroft University of Medical Sciences"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hedyeh","family":"Askarpour","sequence":"additional","affiliation":[{"name":"Jiroft University of Medical Sciences"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3292-2558","authenticated-orcid":false,"given":"Yousef","family":"Baghcheghi","sequence":"additional","affiliation":[{"name":"Jiroft University of Medical Sciences"},{"name":"Jiroft University of Medical Sciences"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","published-online":{"date-parts":[[2026,2,6]]},"reference":[{"key":"e_1_3_3_2_2","volume-title":"World Alzheimer Report 2021. 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