{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,4]],"date-time":"2026-05-04T04:48:17Z","timestamp":1777870097932,"version":"3.51.4"},"reference-count":38,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2026,3,11]],"date-time":"2026-03-11T00:00:00Z","timestamp":1773187200000},"content-version":"vor","delay-in-days":10,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,3,1]],"date-time":"2026-03-01T00:00:00Z","timestamp":1772323200000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82071581"],"award-info":[{"award-number":["82071581"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["CNS Neurosci Ther"],"published-print":{"date-parts":[[2026,3]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Aims<\/jats:title>\n                    <jats:p>Impaired autophagy\u2010mediated clearance of Alzheimer's disease (AD)\u2010related proteins is a critical event in AD pathogenesis. SLC38A9, a member of the Solute Carrier 38 family, acts as an arginine sensor and plays an important role in regulating autophagy. Although the activation of autophagy regulated by the SLC38A9 may have a mitigating effect on AD, this aspect still awaits further exploration.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      APP\/PS1 mouse models and HT22 cells treated with amyloid\u2010\u03b2 25\u201335 (A\u03b2\n                      <jats:sub>25\u201335<\/jats:sub>\n                      ) were transduced with vectors to evaluate the effect of SLC38A9 in AD.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>We show that decreasing SLC38A9 could promote the hippocampal neuronal autophagic clearance of AD\u2010related proteins, reduce neuronal apoptosis, and improve cognitive function.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Our results demonstrate SLC38A9 is involved in AD\u2010related pathology and its cognitive impairment, and may offer new therapeutic targets to AD.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/cns.70823","type":"journal-article","created":{"date-parts":[[2026,3,11]],"date-time":"2026-03-11T13:56:45Z","timestamp":1773237405000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["<scp>SLC38A9<\/scp>\n                    Regulation Affects Hippocampal Neuronal Autophagy: A Potential Alzheimer's Therapeutic Approach by Suppressing Alzheimer's Disease\u2010Related Protein Deposition"],"prefix":"10.1002","volume":"32","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-8852-2572","authenticated-orcid":false,"given":"Yixin","family":"Chen","sequence":"first","affiliation":[{"name":"Department of Geriatrics Huadong Hospital Affiliated 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