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 of USP13 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).

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Document Details

Document Type
Technical Report
Publication Date
Oct 01, 2023
Accession Number
AD1220547

Entities

People

  • Hanseok Ko

Organizations

  • Johns Hopkins University

Tags

Fields of Study

  • Biology

Readers

  • Molecular and Cellular Biology
  • Neurodegenerative Parkinson's Disease and Rickettsial Disease handbook, including the data level of dopamine, BC, neurons, and PD.