Manganese efflux in Parkinsonism: Insights from newly characterized SLC30A10 mutations

Margaret R. DeWitt, Pan Chen, Michael Aschner

Research output: Contribution to journalShort surveypeer-review

37 Scopus citations


Although manganese (Mn) is required for normal cellular function, overexposure to this metal may cause an extrapyramidal syndrome resembling Parkinson's disease (PD). Notably, high whole-blood Mn levels have been reported in patients with idiopathic PD. Because Mn is both essential at low dose and toxic at higher dose; its transport and homeostasis are tightly regulated. Previously, the only protein known to be operant in cellular Mn export was the iron-regulating transporter, ferroportin (Fpn). The causal role for Mn in PD has yet to be fully understood, but evidence of a familial predisposition to PD associated with Mn toxicity is mounting. A recently discovered mutation in SLC30A10 identified its gene product as putatively involved in Mn efflux. Patients with the SLC30A10 mutation display Parkinsonian-like gate disturbances and hypermanganesemia. This review will address Mn transport proteins, the newly discovered SLC30A10 mutations and their implications to Parkinsonism and Mn regulation.

Original languageEnglish (US)
Pages (from-to)1-4
Number of pages4
JournalBiochemical and Biophysical Research Communications
Issue number1
StatePublished - Mar 1 2013
Externally publishedYes


  • Ferroportin 1
  • Iron
  • Manganese
  • Parkinson's disease
  • SLC30A10

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology


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