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Atractylenolide III (AT\u2010III), a terpenoid compound found in medicinal\n                    <jats:italic>Atractylodes macrocephala Koidz<\/jats:italic>\n                    , is well\u2010known for its role in antioxidant and anti\u2010inflammatory activities. The purpose of this study is to explore the beneficial impact of AT\u2010III on AD pathology and identify the mechanisms involved.\n                    <jats:styled-content style=\"fixed-case\">\n                      <jats:italic>C. elegans<\/jats:italic>\n                    <\/jats:styled-content>\n                    CL4176, SH\u2010SY5Y APP\n                    <jats:sub>SWE<\/jats:sub>\n                    , and APP\/PS1 mice were used to investigate the efficacy and possible mechanism of AT\u2010III on the treatment of AD. AT\u2010III reduced amyloid protein (A\u03b2) deposition in\n                    <jats:styled-content style=\"fixed-case\">\n                      <jats:italic>C. elegans<\/jats:italic>\n                    <\/jats:styled-content>\n                    CL4176 heads, prolonged the paralysis time, and reduced A\u03b2 levels in SH\u2010SY5Y APP\n                    <jats:sub>SWE<\/jats:sub>\n                    cells. AT\u2010III improved the learning and memory ability of APP\/PS1 mice and decreased the deposition of A\u03b2 plaques. Transcriptomics and experimental validation showed that AT\u2010III stimulated transcription and translation of autolysosome\u2010associated genes. AT\u2010III enhanced co\u2010localization of LC3 and LAMP2 with A\u03b2 in APP\/PS1 mice. Meanwhile, AT\u2010III increased TFEB transcriptional activity, mRNA, and protein levels in the nucleus. Furthermore, AT\u2010III enhanced the expression of Yin Yang 1 (YY1) protein, an upstream regulator of TFEB, and led to the stimulation of autophagy and lysosome biogenesis both in\u00a0vivo and in\u00a0vitro. The observed effects were reversed upon silencing YY1. AT\u2010III may regulate the YY1\u2010TFEB pathway, thereby restoring autophagy flux disturbances and ameliorating AD\u2010related pathological changes and cognitive decline. This study provides a promising lead compound for intervention in AD.\n                  <\/jats:p>","DOI":"10.1002\/ptr.70069","type":"journal-article","created":{"date-parts":[[2025,8,20]],"date-time":"2025-08-20T11:40:42Z","timestamp":1755690042000},"page":"4474-4490","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":5,"title":["Atractylenolide\n                    <scp>III<\/scp>\n                    Mitigates Alzheimer's Disease by Enhancing Autophagy via the\n                    <scp>YY1<\/scp>\n                    \u2010\n                    <scp>TFEB<\/scp>\n                    Pathway"],"prefix":"10.1002","volume":"39","author":[{"given":"Xiaowei","family":"Zhang","sequence":"first","affiliation":[{"name":"Academy of Chinese Medical Sciences Henan University of Chinese Medicine  Zhengzhou China"},{"name":"Collaborative Innovation Center of Prevention and Treatment of Major Diseases by Chinese and Western Medicine, Henan 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