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Although insulin-degrading enzyme (IDE) has been implicated in both type 2 diabetes mellitus and amyloid-protein clearance, its precise relevance to PD pathogenesis remains unclear. In this study, we show that IDE expression is reduced in the nigrostriatal region of aging homozygous A53T \u03b1-syn mice and in \u03b1-syn-overexpressing SH-SY5Y PD cells. Overexpression of IDE alleviated motor deficits, reduced pathological \u03b1-syn levels, and protected dopaminergic neurons in A53T \u03b1-syn mice. In SH-SY5Y PD model cells, IDE overexpression reduced \u03b1-syn-induced toxicity, whereas IDE knockdown exacerbated it. Integrated transcriptomic and proteomic analyses revealed that the Hippo signaling pathway serves as a major downstream target of IDE. Notably, inhibition of MST1\/2, a pivotal Hippo kinase, recapitulated IDE\u2019s neuroprotective effects by diminishing \u03b1-syn pathology and neuronal apoptosis. Hence, IDE confers neuroprotection partly via suppression of the Hippo signaling pathway, and pharmacological targeting of the IDE-Hippo axis may represent a promising therapeutic strategy for PD.<\/jats:p>","DOI":"10.1038\/s41419-025-08055-4","type":"journal-article","created":{"date-parts":[[2025,10,24]],"date-time":"2025-10-24T15:37:00Z","timestamp":1761320220000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":5,"title":["Insulin-degrading enzyme confers neuroprotection in Parkinson\u2019s disease by inhibiting the Hippo signaling pathway"],"prefix":"10.1038","volume":"16","author":[{"given":"Huimin","family":"Zheng","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yu","family":"Guo","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shuyu","family":"Zhang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yun","family":"Su","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xin","family":"Cui","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhengwei","family":"Hu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaoyan","family":"Hao","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mengjie","family":"Li","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Changhe","family":"Shi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2689-9897","authenticated-orcid":false,"given":"Yuming","family":"Xu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3520-2449","authenticated-orcid":false,"given":"Chengyuan","family":"Mao","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2025,10,24]]},"reference":[{"key":"8055_CR1","doi-asserted-by":"publisher","first-page":"896","DOI":"10.1016\/S0140-6736(14)61393-3","volume":"386","author":"LV Kalia","year":"2015","unstructured":"Kalia LV, Lang AE. 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