Mitochondrial dysfunction in Parkinson’s disease – a key disease hallmark with therapeutic potential

Martin T. Henrich, Wolfgang H. Oertel, D. James Surmeier, Fanni F. Geibl*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

2 Scopus citations

Abstract

Mitochondrial dysfunction is strongly implicated in the etiology of idiopathic and genetic Parkinson’s disease (PD). However, strategies aimed at ameliorating mitochondrial dysfunction, including antioxidants, antidiabetic drugs, and iron chelators, have failed in disease-modification clinical trials. In this review, we summarize the cellular determinants of mitochondrial dysfunction, including impairment of electron transport chain complex 1, increased oxidative stress, disturbed mitochondrial quality control mechanisms, and cellular bioenergetic deficiency. In addition, we outline mitochondrial pathways to neurodegeneration in the current context of PD pathogenesis, and review past and current treatment strategies in an attempt to better understand why translational efforts thus far have been unsuccessful.

Original languageEnglish (US)
Article number83
JournalMolecular neurodegeneration
Volume18
Issue number1
DOIs
StatePublished - Dec 2023

Keywords

  • Antioxidants
  • Electron transport chain
  • MPTP
  • Mitochondria
  • Mitochondrial dysfunction
  • Neuroprotective therapies
  • Parkinson’s disease
  • Synuclein

ASJC Scopus subject areas

  • Clinical Neurology
  • Cellular and Molecular Neuroscience
  • Molecular Biology

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