腦黑質鐵異常沉積、腦內鐵代謝紊亂和鐵促進氧化應激是帕金森患者大腦神經細胞損傷的重要病理生理機制。澳大利亞墨爾本大學的David Finkelstein教授等最新研究發現轉鐵蛋白（transferrin）有助于逆轉帕金森病患者腦內鐵水平的升高。該研究納入10例帕金森病患者和10例無神經疾病歷史的正常對照，其結果顯示帕金森患者大腦黑質平均鐵含量較對照組增高了42%，但轉鐵蛋白水平降低了35%。其細胞實驗進一步發現給予神經元細胞添加轉鐵蛋白可促進其將鐵蛋白轉出細胞。動物實驗提示帕金森小鼠皮下注射轉鐵蛋白可降低其大腦中鐵離子水平，提高其運動能力。然而，轉鐵蛋白也會造成血液中的鐵水平下降導致貧血。盡管該方法這在帕金森病患者中的應用中仍然存在局限，但這一發現為帕金森病的治療指出了新方向。

Treatment with aniron-transporting protein called transferrin could help reverse iron elevationin the Parkinsonian brain. David Finkelstein and colleagues from Australia'sUniversity of Melbourne compared post-mortem samples from 10 people withParkinson's disease and 10 individuals with no history of neurologicalproblems. They found that the substantia nigra region of the brain ofParkinson's patients had a 42% average elevation in iron deposits and a 35%average decrease in transferrin levels compared to the controls. In culturedneurons, adding transferrin helped traffic iron out of the cells. And in amouse model of Parkinson's, transferrin injections under the skin helped loweriron levels in the brain and improve motor symptoms of the disease. However,transferrin also caused iron depletion in the blood, leading to anemia, whichcould limit its therapeutic application in patients.

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.