Cell biology of Parkinson's disease: Mechanisms of synaptic, lysosomal, and mitochondrial dysfunction

Sarah M. Brooker, Grace E. Naylor, Dimitri Krainc*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

3 Scopus citations

Abstract

Parkinson's disease (PD) is a growing cause of disability worldwide and there is a critical need for the development of disease-modifying therapies to slow or stop disease progression. Recent advances in characterizing the genetics of PD have expanded our understanding of the cell biology of this disorder. Mitochondrial oxidative stress, defects in synaptic function, and impaired lysosomal activity have been shown to be linked in PD, resulting in a pathogenic feedback cycle involving the accumulation of toxic oxidized dopamine and alpha-synuclein. In this review, we will highlight recent data on a subset of PD-linked genes which have key roles in these pathways and the pathogenic cycle. We will furthermore discuss findings highlighting the importance of dynamic mitochondria-lysosome contact sites that mediate direct inter-organelle cross-talk in the pathogenesis of PD and related disorders.

Original languageEnglish (US)
Article number102841
JournalCurrent opinion in neurobiology
Volume85
DOIs
StatePublished - Apr 2024

ASJC Scopus subject areas

  • General Neuroscience

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