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Despite globally reduced neural activity during AD onset, recent studies have suggested that A\u03b2 induces hyperexcitability and seizure-like activity during the early stages of the disease that ultimately exacerbate cognitive decline. However, the underlying mechanism is unknown. Here, we reveal an A\u03b2-induced elevation of postsynaptic density protein 95 (PSD-95) in cultured neurons in vitro and in an in vivo AD model using APP\/PS1 mice at 8 weeks of age. Elevation of PSD-95 occurs as a result of reduced ubiquitination caused by Akt-dependent phosphorylation of E3 ubiquitin ligase murine-double-minute 2 (Mdm2). The elevation of PSD-95 is consistent with the facilitation of excitatory synapses and the surface expression of \u03b1-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors induced by A\u03b2. Inhibition of PSD-95 corrects these A\u03b2-induced synaptic defects and reduces seizure activity in APP\/PS1 mice. Our results demonstrate a mechanism underlying elevated seizure activity during early-stage A\u03b2 pathology and suggest that PSD-95 could be an early biomarker and novel therapeutic target for AD.<\/jats:p>","DOI":"10.1038\/s44319-024-00090-0","type":"journal-article","created":{"date-parts":[[2024,2,27]],"date-time":"2024-02-27T06:02:06Z","timestamp":1709013726000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":15,"title":["Hyperfunction of post-synaptic density protein 95 promotes seizure response in early-stage a\u03b2 pathology"],"prefix":"10.1038","volume":"25","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-8839-614X","authenticated-orcid":false,"given":"Yeeun","family":"Yook","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2890-0580","authenticated-orcid":false,"given":"Kwan Young","family":"Lee","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eunyoung","family":"Kim","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Simon","family":"Lizarazo","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1244-0110","authenticated-orcid":false,"given":"Xinzhu","family":"Yu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1032-0107","authenticated-orcid":false,"given":"Nien-Pei","family":"Tsai","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2024,2,27]]},"reference":[{"key":"90_CR1","doi-asserted-by":"publisher","first-page":"1567","DOI":"10.1038\/nn.2433","volume":"12","author":"E Abramov","year":"2009","unstructured":"Abramov E, Dolev I, Fogel H, Ciccotosto GD, Ruff E, Slutsky I (2009) Amyloid-\u03b2 as a positive endogenous regulator of release probability at hippocampal synapses. 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