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Manganese efflux in Parkinsonism: insights from newly characterized SLC30A10 mutations

Margaret R DeWitt1, Pan Chen, Michael Aschner

  • 1Vanderbilt Center for Molecular Toxicology, Department of Pediatrics, Nashville, TN 37232-8552, USA.

Biochemical and Biophysical Research Communications
|January 30, 2013
PubMed

Insights

Manganese (Mn) overexposure can cause Parkinsonism. A newly discovered SLC30A10 mutation reveals a new pathway for manganese export, offering insights into Parkinson's disease and Mn regulation.

Area of Science:

  • Neuroscience
  • Toxicology
  • Genetics

Background:

  • Manganese (Mn) is essential but toxic at high doses, necessitating tight regulation of its transport and homeostasis.
  • High whole-blood Mn levels are observed in idiopathic Parkinson's disease (PD) patients, suggesting a link between Mn and PD.
  • Ferroportin (Fpn) was previously the sole identified protein involved in cellular Mn export.

Purpose of the Study:

  • To review manganese transport proteins.
  • To discuss newly discovered SLC30A10 mutations.
  • To explore the implications of these findings for Parkinsonism and Mn regulation.

Main Methods:

  • Literature review of Mn transport and its role in neurological disorders.
  • Analysis of studies investigating ferroportin (Fpn) in Mn homeostasis.
  • Examination of research on SLC30A10 mutations and associated clinical phenotypes.

Main Results:

  • Evidence suggests familial predisposition to PD linked to Mn toxicity.
  • A mutation in SLC30A10 implicates its gene product in Mn efflux.
  • Patients with SLC30A10 mutations exhibit Parkinsonian symptoms and hypermanganesemia.

Conclusions:

  • SLC30A10 represents a significant protein involved in Mn efflux.
  • Understanding Mn transport mechanisms, including SLC30A10, is crucial for elucidating the causal role of Mn in Parkinsonism.
  • Further research into Mn regulation and transport proteins may reveal novel therapeutic targets for PD.

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