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Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2025,3,4]]},"abstract":"<jats:p>\n                    cAMP response element-binding protein (CREB)-regulated transcription coactivator 1 (CRTC1) plays an important role in synaptic plasticity, learning, and long-term memory formation through the regulation of neuronal activity-dependent gene expression, and CRTC1 dysregulation is implicated in Alzheimer\u2019s disease (AD). Here, we show that increased S-nitrosylation of CRTC1 (forming SNO-CRTC1), as seen in cell-based, animal-based, and human-induced pluripotent stem cell (hiPSC)-derived cerebrocortical neuron-based AD models, disrupts its binding with CREB and diminishes the activity-dependent gene expression mediated by the CRTC1\/CREB pathway. We identified Cys216 of CRTC1 as the primary target of S-nitrosylation by nitric oxide (NO)-related species. Using CRISPR\/Cas9 techniques, we mutated Cys216 to Ala in hiPSC-derived cerebrocortical neurons bearing one allele of the APP\n                    <jats:sup>Swe<\/jats:sup>\n                    mutation (AD-hiPSC neurons). Introduction of this nonnitrosylatable CRTC1 mutant rescued defects in AD-hiPSC neurons, including decreased neurite length and increased neuronal cell death. Additionally, expression of nonnitrosylatable CRTC1 in vivo in the hippocampus rescued synaptic plasticity in the form of long-term potentiation in 5XFAD mice. Taken together, these results demonstrate that formation of SNO-CRTC1 contributes to the pathogenesis of AD by attenuating the neuronal activity-dependent CREB transcriptional pathway, and suggests a therapeutic target for AD.\n                  <\/jats:p>","DOI":"10.1073\/pnas.2418179122","type":"journal-article","created":{"date-parts":[[2025,2,27]],"date-time":"2025-02-27T13:17:31Z","timestamp":1740662251000},"update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":11,"title":["S-Nitrosylation of CRTC1 in Alzheimer\u2019s disease impairs CREB-dependent gene expression induced by neuronal activity"],"prefix":"10.1073","volume":"122","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-6075-6000","authenticated-orcid":false,"given":"Xu","family":"Zhang","sequence":"first","affiliation":[{"name":"Neurodegeneration New Medicines Center and Department of Molecular & Cellular Biology, The Scripps Research Institute","place":["La 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