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Is Chelation Therapy a Potential Treatment for Parkinson's Disease?

Overview
Journal Int J Mol Sci
Publisher MDPI
Date 2021 Apr 3
PMID 33805195
Citations 11
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Abstract

Iron loading in some brain regions occurs in Parkinson's Disease (PD), and it has been considered that its removal by iron chelators could be an appropriate therapeutic approach. Since neuroinflammation with microgliosis is also a common feature of PD, it is possible that iron is sequestered within cells as a result of the "anaemia of chronic disease" and remains unavailable to the chelator. In this review, the extent of neuroinflammation in PD is discussed together with the role played by glia cells, specifically microglia and astrocytes, in controlling iron metabolism during inflammation, together with the results of MRI studies. The current use of chelators in clinical medicine is presented together with a discussion of two clinical trials of PD patients where an iron chelator was administered and showed encouraging results. It is proposed that the use of anti-inflammatory drugs combined with an iron chelator might be a better approach to increase chelator efficacy.

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References
1.
Olivieri N, Nathan D, MacMillan J, Wayne A, Liu P, McGee A . Survival in medically treated patients with homozygous beta-thalassemia. N Engl J Med. 1994; 331(9):574-8. DOI: 10.1056/NEJM199409013310903. View

2.
Oliveira Barbosa J, Santos A, Tumas V, Liu M, Zheng W, Haacke E . Quantifying brain iron deposition in patients with Parkinson's disease using quantitative susceptibility mapping, R2 and R2. Magn Reson Imaging. 2015; 33(5):559-65. DOI: 10.1016/j.mri.2015.02.021. View

3.
Martin-Bastida A, Pietracupa S, Piccini P . Neuromelanin in parkinsonian disorders: an update. Int J Neurosci. 2017; 127(12):1116-1123. DOI: 10.1080/00207454.2017.1325883. View

4.
Cukierman D, Lazaro D, Sacco P, Ferreira P, Diniz R, Fernandez C . X1INH, an improved next-generation affinity-optimized hydrazonic ligand, attenuates abnormal copper(I)/copper(II)-α-Syn interactions and affects protein aggregation in a cellular model of synucleinopathy. Dalton Trans. 2020; 49(45):16252-16267. DOI: 10.1039/d0dt01138j. View

5.
Nathan D . Thalassemia: a look to the future. Ann N Y Acad Sci. 2016; 1368(1):11-5. DOI: 10.1111/nyas.13002. View