{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,25]],"date-time":"2026-09-25T21:04:11Z","timestamp":1790370251333,"version":"4.1.0"},"reference-count":88,"publisher":"Wiley","issue":"29","license":[{"start":{"date-parts":[[2026,3,14]],"date-time":"2026-03-14T00:00:00Z","timestamp":1773446400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,3,14]],"date-time":"2026-03-14T00:00:00Z","timestamp":1773446400000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["advanced.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Advanced Science"],"published-print":{"date-parts":[[2026,5]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    The increasing evidence that non\u2010coding RNAs can become deregulated during pathogenesis is dramatically expanding the space for drug discovery beyond the protein\u2010coding genome. Long noncoding RNAs (lncRNAs) are emerging as key regulators of cellular function, yet most remain uncharacterized. Here, we identify a previously unstudied lncRNA, which we named Neuronal Identity (\n                    <jats:italic>Neuid<\/jats:italic>\n                    ), a conserved, brain\u2010enriched transcript expressed in neurons.\n                    <jats:italic>Neuid<\/jats:italic>\n                    is downregulated in the brains of Alzheimer's disease (AD) patients. Mechanistically,\n                    <jats:italic>Neuid<\/jats:italic>\n                    maintains neuronal identity by repressing developmental and glial genes via interaction with the PRC2 subunit EZH2 and regulation of H3K27me3. Knockdown of\n                    <jats:italic>Neuid<\/jats:italic>\n                    disrupts this repression, leading to impaired neuronal activity and memory formation. Importantly, CRISPRa\u2010mediated\n                    <jats:italic>Neuid<\/jats:italic>\n                    overexpression restores neuronal function in A\u03b242\u2010treated neurons. These findings identify\n                    <jats:italic>NeuID<\/jats:italic>\n                    as a critical regulator of neuronal plasticity and position it as a promising therapeutic target for AD\n                  <\/jats:p>","DOI":"10.1002\/advs.202514972","type":"journal-article","created":{"date-parts":[[2026,3,14]],"date-time":"2026-03-14T19:19:27Z","timestamp":1773515967000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Neuid: A Novel Neuron\u2010Enriched LncRNA that Connects Epigenetic Gene Silencing to Alzheimer's Disease"],"prefix":"10.1002","volume":"13","author":[{"given":"Ranjit","family":"Pradhan","sequence":"first","affiliation":[{"name":"Department For Epigenetics and Systems Medicine in Neurodegenerative Diseases German Center for Neurodegenerative Diseases (DZNE)  G\u00f6ttingen Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zorica","family":"Petrovic","sequence":"additional","affiliation":[{"name":"Dominick P. 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