{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,2,21]],"date-time":"2025-02-21T12:49:14Z","timestamp":1740142154434,"version":"3.37.3"},"reference-count":53,"publisher":"Bentham Science Publishers Ltd.","issue":"3","funder":[{"DOI":"10.13039\/100000957","name":"American Alzheimer Association Grant","doi-asserted-by":"publisher","award":["NIRG-12-237009"],"award-info":[{"award-number":["NIRG-12-237009"]}],"id":[{"id":"10.13039\/100000957","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["eurekaselect.com"],"crossmark-restriction":true},"short-container-title":["CAR"],"published-print":{"date-parts":[[2020,5,18]]},"abstract":"<jats:sec>\n<jats:title>Background:<\/jats:title>\n<jats:p>Clinical evidence indicates that patients affected by Alzheimer's Disease (AD)\nfail to form new memories although their memories for old events are intact. This amnesic pattern depends\non the selective vulnerability to AD-neurodegeneration of the hippocampus, the brain region that\nsustains the formation of new memories, while cortical regions that store remote memories are spared.<\/jats:p>\n<\/jats:sec>\n<jats:sec>\n<jats:title>Objective:<\/jats:title>\n<jats:p>To identify the cellular mechanisms underlying impaired recent memories and intact remote\nmemories in a mouse model of AD.<\/jats:p>\n<\/jats:sec>\n<jats:sec>\n<jats:title>Method:<\/jats:title>\n<jats:p>Glutamatergic synaptic currents were recorded by patch-clamp in acute hippocampal and\nanterior Cingulate Cortical (aCC) slices of AD-like Tg2576 mice and Wild-type (Wt) littermates subjected\nto the Contextual Fear Conditioning (CFC) task or in na\u00efve conditions.<\/jats:p>\n<\/jats:sec>\n<jats:sec>\n<jats:title>Results:<\/jats:title>\n<jats:p>Glutamatergic synaptic currents were recorded by patch-clamp in acute hippocampal and\nanterior Cingulate Cortical (aCC) slices of AD-like Tg2576 mice and Wild-type (Wt) littermates subjected\nto the Contextual Fear Conditioning (CFC) task or in na\u00efve conditions.<\/jats:p>\n<\/jats:sec>\n<jats:sec>\n<jats:title>Conclusion:<\/jats:title>\n<jats:p>Our data suggest that in the early AD stages synaptic plasticity of CA1 synapses, crucial\nto form new memories, is lost, while plasticity of aCC synapses is intact and contributes to the persistence\nof long-term memories.<\/jats:p>\n<\/jats:sec>","DOI":"10.2174\/1567205017666200224122113","type":"journal-article","created":{"date-parts":[[2020,2,24]],"date-time":"2020-02-24T14:21:24Z","timestamp":1582554084000},"page":"259-268","update-policy":"https:\/\/doi.org\/10.2174\/bsp_crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["Synaptic Correlates of Anterograde Amnesia and Intact Retrograde Memory in a Mouse Model of Alzheimer\u2019s Disease"],"prefix":"10.2174","volume":"17","author":[{"given":"Emanuela","family":"Rizzello","sequence":"first","affiliation":[{"name":"European Brain Research Institute (EBRI), Fondazione Rita Levi-Montalcini, Via Regina Elena 295, 00161, Rome, Italy"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Silvia","family":"Middei","sequence":"additional","affiliation":[{"name":"Consiglio Nazionale delle Ricerche (CNR), Institute of Biochemistry and Cell Biology, Via E. 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