{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,16]],"date-time":"2026-06-16T10:52:19Z","timestamp":1781607139271,"version":"3.54.5"},"reference-count":34,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2026,4,9]],"date-time":"2026-04-09T00:00:00Z","timestamp":1775692800000},"content-version":"vor","delay-in-days":8,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,4,1]],"date-time":"2026-04-01T00:00:00Z","timestamp":1775001600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/100032579","name":"Beijing Medical Award Foundation","doi-asserted-by":"publisher","award":["YXJL\u20102022\u20100351\u20100412"],"award-info":[{"award-number":["YXJL\u20102022\u20100351\u20100412"]}],"id":[{"id":"10.13039\/100032579","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Journal of Neurochemistry"],"published-print":{"date-parts":[[2026,4]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>The chronic accumulation of \u0394FosB in striatal medium spiny neurons has been implicated as a pivotal contributor to the pathogenesis of levodopa\u2010induced dyskinesia (LID). While recent studies have implicated autophagy in the degradation of \u0394FosB and the amelioration of LID, the precise mechanisms remain elusive. We induced LID in a unilateral 6\u2010hydroxydopamine\u2010lesioned parkinsonism rat model via chronic levodopa treatment. To modulate the autophagy pathway, we overexpressed ATG14 in the striatum of LID rats and administered chloroquine, an autophagy inhibitor, peripherally. We assessed LID severity using abnormal involuntary movements (AIMs) scores. Western blotting, real\u2010time quantitative polymerase chain reaction, immunofluorescence, immunohistochemistry, transmission electron microscopy, and Golgi staining were employed to measure autophagy flux, synaptic alterations, and \u0394FosB levels. Chronic levodopa treatment reduced ATG14 and SNARE complex (STX17, SNAP29, and VAMP8) levels, disrupted their interaction, impaired autophagy flux, affected synaptic function, and led to \u0394FosB accumulation in the striatum of PD rats. Upregulating ATG14 in the striatum of LID rats improved AIMs scores, facilitated SNARE\u2010mediated autophagosome\u2010lysosome fusion, restored synaptic deficits, and promoted \u0394FosB degradation. However, these beneficial effects of ATG14 upregulation were negated by chloroquine administration. Our findings suggest that upregulating ATG14 enhances SNARE formation, promoting autophagy flux and thereby reducing LID occurrence by facilitating \u0394FosB degradation.<\/jats:p>\n                  <jats:p>\n                    <jats:boxed-text content-type=\"graphic\" position=\"anchor\">\n                      <jats:graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" mimetype=\"image\/png\" position=\"anchor\" specific-use=\"enlarged-web-image\" xlink:href=\"graphic\/jnc70431-gra-0001-m.png\">\n                        <jats:alt-text>image<\/jats:alt-text>\n                      <\/jats:graphic>\n                    <\/jats:boxed-text>\n                  <\/jats:p>","DOI":"10.1111\/jnc.70431","type":"journal-article","created":{"date-parts":[[2026,4,9]],"date-time":"2026-04-09T09:45:01Z","timestamp":1775727901000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["<scp>ATG14<\/scp>\n                    \u2010Mediated\n                    <scp>SNARE<\/scp>\n                    Complex Activation Promotes\n                    <scp>\u0394FosB<\/scp>\n                    Degradation to Ameliorate Levodopa\u2010Induced Dyskinesia"],"prefix":"10.1111","volume":"170","author":[{"given":"Yi","family":"Wu","sequence":"first","affiliation":[{"name":"Department of Neurology Union Hospital, Tongji Medical College, Huazhong University of Science and Technology  Wuhan Hubei China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ke","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Neurology Jiangsu Province Hospital of Chinese Medicine, Affiliated Hospital of Nanjing University of Chinese Medicine  Nanjing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhaoyuan","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of Neurology the First Medical Center, Chinese PLA General Hospital  Beijing 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