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We have previously expressed the full\u2010length human APP in <jats:italic>Drosophila<\/jats:italic> and established a fly AD model that exhibits multiple AD\u2010like symptoms. Here we report that depletion of <jats:italic>CHIP<\/jats:italic> effectively palliated APP\u2010induced pathological symptoms, including morphological, behavioral, and cognitive defects. Mechanistically, CHIP is required for APP\u2010induced autophagy dysfunction, which promotes A\u03b2 production via increased expression of <jats:italic>BACE<\/jats:italic> and <jats:italic>Psn<\/jats:italic>. Our findings suggest that aberrant autophagy is not only a consequence of abnormal APP activity, but also contributes to dysregulated APP metabolism and subsequent AD pathogenesis.<\/jats:p>","DOI":"10.1111\/acel.13070","type":"journal-article","created":{"date-parts":[[2019,11,28]],"date-time":"2019-11-28T08:57:03Z","timestamp":1574931423000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":17,"title":["<i>CHIP<\/i> modulates APP\u2010induced autophagy\u2010dependent pathological symptoms in <i>Drosophila<\/i>"],"prefix":"10.1111","volume":"19","author":[{"given":"Luming","family":"Zhuang","sequence":"first","affiliation":[{"name":"The First Rehabilitation Hospital of Shanghai Shanghai Key Laboratory of Signaling and Diseases Research School of Life Science and Technology Tongji University Shanghai 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