USP13-Mediated Dopaminergic Neurodegeneration
Abstract
We hypothesize that USP13 contributes to dopaminergic neurodegeneration and mitochondrial dysfunction in PD through dysregulation of parkin stability and function and that USP13 could be a potential therapeutic target for PD. To address our hypothesis, we propose 1) To determine whether USP13 depletion leads to dopaminergic neurodegeneration, LBs pathology, and motor and mitochondria defects in vivo (Specific Aim 1), 2) To determine the effects ofUSP13 manipulation (overexpression or depletion) in dopaminergic neurodegeneration, LBs-like pathology, and mitochondrial dysfunction induced by 6-OHDA or alpha-synuclein PFF in human dopaminergic neurons (Specific Aim 2), 3) To determine the effects of USP13 manipulation(overexpression or depletion) in dopaminergic neurodegeneration, LBs-like pathology, and motor and mitochondria defects in the 6-OHDA mouse model or the alpha-synuclein PFF mouse model (Specific Aim 3).
Document Details
- Document Type
- Technical Report
- Publication Date
- Oct 01, 2022
- Accession Number
- AD1191291
Entities
People
- Hanseok Ko
Organizations
- Johns Hopkins University