Endolysosomal dysfunction in Parkinson's disease: Recent developments and future challenges

Lauren R. Kett, William T. Dauer

Research output: Contribution to journalArticle

13 Scopus citations

Abstract

Increasingly, genetic, cell biological, and in vivo work emphasizes the role of the endolysosomal system dysfunction in Parkinson's disease pathogenesis. Yet many questions remain about the mechanisms by which primary endolysosomal dysfunction causes PD as well as how the endolysosomal system interacts with α-synuclein-mediated neurotoxicity. We recently described a new mouse model of parkinsonism in which loss of the endolysosomal protein Atp13a2 causes behavioral, neuropathological, and biochemical changes similar to those present in human subjects with ATP13A2 mutations. In this Scientific Perspectives, we revisit the evidence implicating the endolysosomal system in PD, current hypotheses of disease pathogenesis, and how recent studies refine these hypotheses and raise new questions for future research.

Original languageEnglish (US)
Pages (from-to)1433-1443
Number of pages11
JournalMovement Disorders
Volume31
Issue number10
DOIs
StatePublished - Oct 1 2016
Externally publishedYes

Keywords

  • Atp13a2
  • endolysosomal system
  • Kufor-Rakeb syndrome
  • Parkinson's disease

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology

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