MassIVE MSV000098209

Complete Public PXD065038

Neuronal Idol deletion ameliorates amyloid pathology

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Description

Earlier studies demonstrated that overexpression of the low-density lipoprotein receptor (LDLR) decreases apolipoprotein E (APOE) levels in the brain and alleviates amyloid-beta (Abeta) pathology. We hypothesized that inhibiting the Inducible Degrader of LDLR (IDOL)- an E3 ubiquitin ligase that ubiquitinates LDLR for degradation- would increase endogenous LDLR levels and decrease amyloid pathology. Previously, we demonstrated that the deletion of Idol increased LDLR levels and reduced amyloid deposition in a transgenic mouse model of Abeta-amyloidosis. However, the cellular mechanisms underlying these beneficial effects were unknown. Here, we investigate the cell-type-specific contribution of Idol deletion to amyloid pathology by generating Idol conditional knock-out mouse models. We demonstrate that deletion of neuronal, but not microglial, Idol reduces amyloid accumulation in the 5XFAD transgenic mouse model. Furthermore, only neuronal Idol deletion alters brain LDLR and APOE levels, pointing to the critical role of the neuronal LDLR-APOE axis in modulating Abeta accumulation. [doi:10.25345/C56H4D349] [dataset license: CC0 1.0 Universal (CC0 1.0)]

Keywords: Idol ; APOE ; LDLR ; VLDLR ; Reelin ; Abeta ; DatasetType:Proteomics

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Principal Investigators:
(in alphabetical order) 		Jungsu Kim, Indiana University School of Medicine, United States of America
Submitting User: JungsuKimLab
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