Title: Manganese efflux in Parkinsonism: insights from newly characterized SLC30A10 mutations.

Authors: DeWitt, Margaret R; Chen, Pan; Aschner, Michael

Published In Biochem Biophys Res Commun, (2013 Mar 01)

Abstract: 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.

PubMed ID: 23357421

MeSH Terms: Cation Transport Proteins/genetics*; Humans; Ion Transport; Manganese/blood; Manganese/metabolism*; Mutation; Parkinsonian Disorders/blood; Parkinsonian Disorders/genetics*; Parkinsonian Disorders/metabolism*; Zinc Transporter 8