{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T22:26:45Z","timestamp":1791239205587,"version":"4.1.0"},"reference-count":55,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"1","license":[{"start":{"date-parts":[[2024,7,29]],"date-time":"2024-07-29T00:00:00Z","timestamp":1722211200000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-sa\/4.0"}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2026,1]]},"abstract":"<jats:p>JOURNAL\/nrgr\/04.03\/01300535-202601000-00042\/figure1\/v\/2026-04-22T161640Z\/r\/image-tiff<\/jats:p>\n                  <jats:p>\n                    Long noncoding RNA and microRNA are regulatory noncoding RNAs that are implicated in Alzheimer\u2019s disease, but the role of long noncoding RNA-associated competitive endogenous RNA has not been fully elucidated. The long noncoding RNA growth arrest-specific 5 (GAS5) is a member of the 5\u2032-terminal oligopyrimidine gene family that may be involved in neurological disorders, but its role in Alzheimer\u2019s disease remains unclear. This study aimed to investigate the function of GAS5 and construct a GAS5-associated competitive endogenous RNA network comprising potential targets. RNA sequencing results showed that GAS5 was upregulated in five familial Alzheimer\u2019s disease (5\u00d7FAD) mice, APPswe\/PSEN1dE9 (APP\/PS1) mice, Alzheimer\u2019s disease-related APPswe cells, and serum from patients with Alzheimer\u2019s disease. Functional experiments with targeted overexpression and silencing demonstrated that GAS5 played a role in cognitive dysfunction and multiple Alzheimer\u2019s disease-associated pathologies, including tau hyperphosphorylation, amyloid-beta accumulation, and neuronal apoptosis. Mechanistic studies indicated that GAS5 acted as an endogenous sponge by competing for microRNA-23b-3p (miR-23b-3p) binding to regulate its targets glycogen synthase kinase 3beta (GSK-3\u03b2) and phosphatase and tensin homologue deleted on chromosome 10 (PTEN) expression in an Argonaute 2-induced RNA silencing complex (RISC)-dependent manner. GAS5 inhibited miR-23b-3p-mediated GSK-3\u03b2 and PTEN cascades with a feedforward PTEN\/protein kinase B (Akt)\/GSK-3\u03b2 linkage. Furthermore, recovery of GAS5\/miR-23b-3p\/GSK-3\u03b2\/PTEN pathways relieved Alzheimer\u2019s disease-like symptoms\n                    <jats:italic toggle=\"yes\">in vivo<\/jats:italic>\n                    , indicated by the amelioration of spatial cognition, neuronal degeneration, amyloid-beta load, and tau phosphorylation. Together, these findings suggest that GAS5 promotes Alzheimer\u2019s disease pathogenesis. This study establishes the functional convergence of the GAS5\/miR-23b-3p\/GSK-3\u03b2\/PTEN pathway on multiple pathologies, suggesting a candidate therapeutic target in Alzheimer\u2019s disease.\n                  <\/jats:p>","DOI":"10.4103\/nrr.nrr-d-23-01273","type":"journal-article","created":{"date-parts":[[2024,8,6]],"date-time":"2024-08-06T09:13:11Z","timestamp":1722935591000},"page":"392-405","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":10,"title":["Long noncoding RNA GAS5 acts as a competitive endogenous RNA to regulate GSK-3\u03b2 and PTEN expression by sponging miR-23b-3p in Alzheimer\u2019s disease"],"prefix":"10.4103","volume":"21","author":[{"given":"Li","family":"Zeng","sequence":"first","affiliation":[{"name":"Institute of Medicinal Biotechnology, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China"},{"name":"State Key Laboratory of Bioactive Substances and Functions of 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and Peking Union Medical College, Beijing, China"},{"name":"State Key Laboratory of Bioactive Substances and Functions of Natural Medicines, Institute of Medicinal Biotechnology, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5748-7444","authenticated-orcid":false,"given":"Zhuorong","family":"Li","sequence":"additional","affiliation":[{"name":"Institute of Medicinal Biotechnology, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China"},{"name":"State Key Laboratory of Bioactive Substances and Functions of Natural Medicines, Institute of Medicinal Biotechnology, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, 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