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Iron deposition in Parkinson’s disease (PD) is a potential disease-modifying target. We previously showed that supplementation of the iron-exporter, ceruloplasmin, selectively corrected nigral iron elevation in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) model. Ceruloplasmin delivers iron to transferrin (Tf), the extracellular iron-transporting protein. We show that Tf protein levels are decreased in the nigra of post-mortem PD brains compared with controls (−35%;  n =10 each). Because Tf traffics iron away from iron-replete tissues, we hypothesized that Tf supplementation could selectively facilitate iron export from the nigra in PD. In cultured neurons, Tf treatment corrected iron accumulation, and subcutaneous Tf to mice ameliorated iron accumulation and motor deficits in the MPTP model of PD. Although these data support a role for Tf in the disease mechanism for PD, and its potential use for correcting disorders of iron overload, Tf therapy also caused systemic iron depletion, which could limit its application for PD.

Transferrin protects against Parkinsonian neurotoxicity and is deficient in Parkinson’s substantia nigra