Cited by 173Parkinson's Disease Mechanisms and TreatmentsIron Metabolism and DisordersGenetic Associations and Epidemiology

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Serum Iron Levels and the Risk of Parkinson Disease: A Mendelian Randomization Study

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Pichler, Irene, Del Greco M., Fabiola, Gögele, Martin, Lill, Christina M., Bertram, Lars, Do, Chuong B., Eriksson, Nicholas, Foroud, Tatiana, Myers, Richard H., PD GWAS Consortium, Nalls, Michael, Keller, Margaux F., International Parkinson's Disease Genomics Consortium, Wellcome Trust Case Control Consortium 2, Benyamin, Beben, Whitfield, John B., Genetics of Iron Status Consortium, Pramstaller, Peter P., Hicks, Andrew A., Thompson, John R., Minelli, Cosetta·2013·PLoS Medicine

DOI 10.1371/journal.pmed.1001462PMC PMC3672214

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Abstract

BACKGROUND: Although levels of iron are known to be increased in the brains of patients with Parkinson disease (PD), epidemiological evidence on a possible effect of iron blood levels on PD risk is inconclusive, with effects reported in opposite directions. Epidemiological studies suffer from problems of confounding and reverse causation, and mendelian randomization (MR) represents an alternative approach to provide unconfounded estimates of the effects of biomarkers on disease. We performed a MR study where genes known to modify iron levels were used as instruments to estimate the effect of iron on PD risk, based on estimates of the genetic effects on both iron and PD obtained from the largest sample meta-analyzed to date. METHODS AND FINDINGS: We used as instrumental variables three genetic variants influencing iron levels, HFE rs1800562, HFE rs1799945, and TMPRSS6 rs855791. Estimates of their effect on serum iron were based on a recent genome-wide meta-analysis of 21,567 individuals, while estimates of their effect on PD risk were obtained through meta-analysis of genome-wide and candidate gene studies with 20,809 PD cases and 88,892 controls. Separate MR estimates of the effect of iron on PD were obtained for each variant and pooled by meta-analysis. We investigated heterogeneity across the three estimates as an indication of possible pleiotropy and found no evidence of it. The combined MR estimate showed a statistically significant protective effect of iron, with a relative risk reduction for PD of 3% (95% CI 1%-6%; p = 0.001) per 10 µg/dl increase in serum iron. CONCLUSIONS: Our study suggests that increased iron levels are causally associated with a decreased risk of developing PD. Further studies are needed to understand the pathophysiological mechanism of action of serum iron on PD risk before recommendations can be made.

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Figure 1 Graphical representation of the MR approach, with all estimates used to derive the final MR estimate. *Reported is the allele that increases iron levels, together with its frequency (AF). **This corresponds approximately to an OR per unit µg/dl increase in iron of 0.997 (95%CI 0.994–0.999), that is 0.3% (0.1%–0.6%) relative reduction in PD risk per 1 µg/dl increase in iron.CC BY · PubMed Central

Figure 2 Forest plot of the MR estimates from the three instruments. The size of the squares is proportional to the precision of the MR estimates for each polymorphism, with the horizontal lines indicating their 95% confidence intervals. The combined MR estimate is represented by the centre of the diamond, with the lateral tips indicating its 95% confidence interval. The solid vertical line is the line of no effect.CC BY · PubMed Central

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Measuring inconsistency in meta-analyses
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Background
Using multiple genetic variants as instrumental variables for modifiable risk factors
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BackgroundInfluential
The serine protease TMPRSS6 is required to sense iron deficiency
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Background
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The Hemochromatosis Founder Mutation in HLA-H Disrupts β2-Microglobulin Interaction and Cell Surface Expression
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MethodSelf-citation
Genome-wide genotyping in Parkinson's disease and neurologically normal controls: first stage analysis and public release of data
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Method
Echogenicity of the Substantia Nigra
Berg, D., Roggendorf, W., Schroeder, U., Klein, R., Tatschner, T., Benz, P. M., Tucha, O. M., Preier, M., Lange, K. W., Reiners, K., et al. (2002) · Archives of Neurology · doi:10.1001/archneur.59.6.999 · Cited by 381 · cited 1×
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Background
Hereditary hemochromatosis: Effects of C282Y and H63D mutations on association with β 2 -microglobulin, intracellular processing, and cell surface expression of the HFE protein in COS-7 cells
Waheed, A., Parkkila, S., Zhou, X. Y., Tomatsu, S., Tsuchihashi, Z., Feder, J. N., Schatzman, R. C., Britton, R. S., Bacon, B. R., & Sly, W. S. (1997) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.94.23.12384 · Cited by 380 · cited 1×
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Pooled analysis of tobacco use and risk of Parkinson disease.
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Cord serum ferritin concentrations and mental and psychomotor development of children at five years of age
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Massachusetts General Hospital
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Effect of Tea and Other Dietary Factors on Iron Absorption
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A Two-Stage Meta-Analysis Identifies Several New Loci for Parkinson's Disease
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The discovery of the new haemochromatosis gene
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Background
Meta-analysis of Parkinson disease: Identification of a novel locus, RIT2
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Common variants in TMPRSS6 are associated with iron status and erythrocyte volume
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BackgroundInfluential
Assumptions of IV Methods for Observational Epidemiology.
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Inhibition of food iron absorption by coffee
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Background
Iron dysregulation in movement disorders
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“accumulation in the brain of PD patients [2,3], epidemiological”
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Neonatal Iron Deficiency Results in Irreversible Changes in Dopamine Function in Rats
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Background
Re: Estimation of Bias in Nongenetic Observational Studies Using “Mendelian Triangulation” by Bautista et al.
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Self-citation
The University of Texas Southwestern Medical Center
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Association study between iron-related genes polymorphisms and Parkinson's disease
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Result
In vitro and in vivo studies investigating possible antioxidant actions of nicotine: relevance to Parkinson's and Alzheimer's diseases.
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Background
THE CLEVELAND CLINIC FOUNDATION
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TMPRSS6 rs855791 modulates hepcidin transcription in vitro and serum hepcidin levels in normal individuals
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Background
Genetics of iron regulation and the possible role of iron in Parkinson's disease
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“Among the many genes evaluated, which include FTL, FTH1, TF, TFRC, IREB2, LTF, CP, FXN, HFE [52], HPX, HAMP, HFE2 [53], and FTMT [54], only the G258S polymorphism in the TF gene showed a statistically significant association with PD [17], although the finding was not replicated in a subsequent study [55], and a haplot…”
Result
Characterization of the Active Site Iron in Tyrosine Hydroxylase
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“Low peripheral iron levels may reduce the functioning of neuronal enzymes or receptors, since iron is a crucial cofactor of tyrosine hydroxylase [49], plays a role in the synthesis of monoamine neurotransmitters, and is involved in dopaminergic neurodevelopment [50].”
Background
TMPRSS6, but not TF, TFR2 or BMP2 variants are associated with increased risk of iron-deficiency anemia
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Background
Dietary intake of metals and risk of Parkinson's disease: A case-control study in Japan
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Result
Association of HFE common mutations with Parkinson's disease, Alzheimer's disease and mild cognitive impairment in a Portuguese cohort
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“our analysis for both rs1800562 [13–20] and rs1799945 [13– 17,19–21] (Tables 1 and S2).”
Mutations in the hemochromatosis gene (HFE), Parkinson's disease and parkinsonism
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“our analysis for both rs1800562 [13–20] and rs1799945 [13– 17,19–21] (Tables 1 and S2).”
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Iron and ageing: an introduction to iron regulatory mechanisms
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“Furthermore, low iron levels may decrease neuronal iron storage in the form of ferritin [51], which was found to be inappropriately low in SN neurons in PD [1].”
Background
Fe and Cu do not differ in Parkinson's disease: a replication study plus meta-analysis.
Mariani, S., Ventriglia, M., Simonelli, I., Donno, S., Bucossi, S., Vernieri, F., Melgari, J., Pasqualetti, P., Rossini, P., & Squitti, R. (2013) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2012.05.015 · Cited by 73 · cited 2×
“heterogeneity across studies [6].”
Estimation of Bias in Nongenetic Observational Studies Using “Mendelian Triangulation”
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“using the Delta method [33,34].”
ANEMIA OR LOW HEMOGLOBIN LEVELS PRECEDING PARKINSON DISEASE: A CASE-CONTROL STUDY
Kasten, M., Tadić, V., Klein, C., Rocca, W., Savica, R., Ahlskog, J., & Grossardt, B. (2010) · Neurology · doi:10.1212/wnl.0b013e3181d8a3d6 · Cited by 66 · cited 1×
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Background
Role of dietary iron restriction in a mouse model of Parkinson's disease
Levenson, C. W., Cutler, R. G., Ladenheim, B., Cadet, J. L., Hare, J., & Mattson, M. P. (2004) · Experimental Neurology · doi:10.1016/j.expneurol.2004.08.014 · Cited by 64 · cited 2×
“A reduction in ferritin could decrease neuronal iron utilization by decreasing the pool of iron available for neuronal enzymes [47], thus leading to the accumulation of free iron in SN [1].”
Background
Hereditary haemochromatosis mutation frequencies in the general population
Bradley, L., Johnson, D. D., Palomaki, G., Haddow, J., Robertson, N. H., & Ferrie, R. (1998) · Journal of Medical Screening · doi:10.1136/jms.5.1.34 · Cited by 58 · cited 1×
“The two variants in the HFE gene are responsible for most cases of hereditary hemochromatosis [59,60], and they are associated with iron overload when present in the homozygous (C282Y/C282Y) or compound heterozygous (C282Y/H63D) state.”
Background
The Cys282Tyr polymorphism in the HFE gene in Australian Parkinson's disease patients
Buchanan, D. D., Silburn, P. A., Chalk, J. B., Couteur, D. G. L., & Mellick, G. D. (2002) · Neuroscience Letters · doi:10.1016/s0304-3940(02)00398-1 · Cited by 57 · cited 3×
“our analysis for both rs1800562 [13–20] and rs1799945 [13– 17,19–21] (Tables 1 and S2).”
Method
DMT1 polymorphism and risk of Parkinson's disease.
He, Q., Du, T., Yu, X., Xie, A., Song, N., Kang, Q., Yu, J.-T., Tan, L., Xie, J.-X., & Jiang, H. (2011) · Neuroscience Letters · doi:10.1016/j.neulet.2011.07.001 · Cited by 57 · cited 1×
“Among the many genes evaluated, which include FTL, FTH1, TF, TFRC, IREB2, LTF, CP, FXN, HFE [52], HPX, HAMP, HFE2 [53], and FTMT [54], only the G258S polymorphism in the TF gene showed a statistically significant association with PD [17], although the finding was not replicated in a subsequent study [55], and a haplot…”
Result
Screening for mutations of the HFE gene in Parkinson's disease patients with hyperechogenicity of the substantia nigra.
Akbas, N., Hochstrasser, H., Deplazes, J., Tomiuk, J., Bauer, P., Walter, U., Behnke, S., Riess, O., & Berg, D. (2006) · Neuroscience Letters · doi:10.1016/j.neulet.2006.07.070 · Cited by 48 · cited 2×
“our analysis for both rs1800562 [13–20] and rs1799945 [13– 17,19–21] (Tables 1 and S2).”
Severity of bias of a simple estimator of the causal odds ratio in Mendelian randomization studies
Harbord, R. M., Didelez, V., Palmer, T., Meng, S., Sterne, J. A. C., & Sheehan, N. A. (2012) · Statistics in Medicine · doi:10.1002/sim.5659 · Cited by 46
Prevalence of haemochromatosis gene mutations in Parkinson’s disease
Aamodt, A., Stovner, L., Thorstensen, K., Lydersen, S., White, L., & Aasly, J. (2006) · Journal of Neurology Neurosurgery & Psychiatry · doi:10.1136/jnnp.2006.101352 · Cited by 40 · cited 1×
“performing a per-genotype analysis based on an additive genetic model [19], or a per-allele analysis when genotype data were not available [20].”
Method
Neuroprotection by the multitarget iron chelator M30 on age-related alterations in mice
Kupershmidt, L., Amit, T., Bar‐Am, O., Youdim, M. B. H., & Weinreb, O. (2012) · Mechanisms of Ageing and Development · doi:10.1016/j.mad.2012.03.001 · Cited by 40 · cited 1×
“MAO inhibitors may have iron-chelating effects and thus reduce iron blood levels, which could lead to spurious epidemiological evidence of a difference in iron levels between PD cases and controls [42].”
Background
Blood donations, iron stores, and risk of Parkinson's disease
Logroscino, G., Chen, H., Wing, A., & Ascherio, A. (2006) · Movement Disorders · doi:10.1002/mds.20826 · Cited by 38 · cited 1×
“A case-control study suggested an increased risk of PD in men who reported multiple recent blood donations and thus experienced depleted systemic iron stores [45], and another study showed an association of anemia experienced early in life with increased PD risk, with the authors hypothesizing that anemia could be a s…”
Background
Mount Sinai School of Medicine.
Stagnaro-Green, A., & Smith, L. G. (2000) · Academic medicine : journal of the Association of American Medical Colleges · doi:10.1097/00001888-200009001-00070 · Cited by 30
HFE gene mutations in a population of Italian Parkinson's disease patients.
Biasiotto, G., Goldwurm, S., Finazzi, D., Tunesi, S., Zecchinelli, A., Sironi, F., Pezzoli, G., & Arosio, P. (2008) · Parkinsonism & Related Disorders · doi:10.1016/j.parkreldis.2007.10.011 · Cited by 28 · cited 1×
“performing a per-genotype analysis based on an additive genetic model [19], or a per-allele analysis when genotype data were not available [20].”
Method
Genetic predisposition to Parkinson's disease: CYP2D6 and HFE in the Faroe Islands
Halling, J., Petersen, M. S., Grandjean, P., Weihe, P., & Brøsen, K. (2008) · Pharmacogenetics & Genomics · doi:10.1097/fpc.0b013e3282f5106e · Cited by 28 · cited 2×
“our analysis for both rs1800562 [13–20] and rs1799945 [13– 17,19–21] (Tables 1 and S2).”
Substantia nigra echogenicity in Parkinson’s disease: relation to serum iron and C-reactive protein
Walter, U., Witt, R., Wolters, A., Wittstock, M., & Benecke, R. (2011) · Journal of neural transmission · doi:10.1007/s00702-011-0664-z · Cited by 17 · cited 1×
“A recent study showed a negative correlation between SN echogenicity, a marker for increased SN iron content [43], and serum iron levels in PD patients [44].”
Background
Association study between four polymorphisms in the HFE, TF and TFR genes and Parkinson’s disease in Southern Italy
Greco, V., Marco, E. V. D., Rocca, F., Annesi, F., Civitelli, D., Provenzano, G., Tarantino, P., Scornaienchi, V., Pucci, F., Salsone, M., et al. (2011) · Neurological Sciences · doi:10.1007/s10072-011-0504-9 · Cited by 16 · cited 2×
“our analysis for both rs1800562 [13–20] and rs1799945 [13– 17,19–21] (Tables 1 and S2).”
Sequence Variations in Mitochondrial Ferritin: Distribution in Healthy Controls and Different Types of Patients
Castiglioni, E., Finazzi, D., Goldwurm, S., Levi, S., Pezzoli, G., Garavaglia, B., Nardocci, N., Malcovati, L., della Porta, M. D., Gallì, A., et al. (2010) · Genetic Testing and Molecular Biomarkers · doi:10.1089/gtmb.2010.0076 · Cited by 16 · cited 2×
“Among the many genes evaluated, which include FTL, FTH1, TF, TFRC, IREB2, LTF, CP, FXN, HFE [52], HPX, HAMP, HFE2 [53], and FTMT [54], only the G258S polymorphism in the TF gene showed a statistically significant association with PD [17], although the finding was not replicated in a subsequent study [55], and a haplot…”
Result
Analysis of Nucleotide Variations in Genes of Iron Management in Patients of Parkinson's Disease and Other Movement Disorders
Castiglioni, E., Finazzi, D., Goldwurm, S., Pezzoli, G., Forni, G., Girelli, D., Maccarinelli, F., Poli, M., Ferrari, M., Cremonesi, L., et al. (2010) · Parkinson's Disease · doi:10.4061/2011/827693 · Cited by 12 · cited 2×
“Among the many genes evaluated, which include FTL, FTH1, TF, TFRC, IREB2, LTF, CP, FXN, HFE [52], HPX, HAMP, HFE2 [53], and FTMT [54], only the G258S polymorphism in the TF gene showed a statistically significant association with PD [17], although the finding was not replicated in a subsequent study [55], and a haplot…”
Result
Association study of the G258S transferrin gene polymorphism and Parkinson's disease in the Spanish population
Ezquerra, M., Campdelacreu, J., Muñóz, E., & Tolosa, E. (2005) · Journal of Neurology · doi:10.1007/s00415-005-0695-1 · Cited by 11 · cited 1×
“Among the many genes evaluated, which include FTL, FTH1, TF, TFRC, IREB2, LTF, CP, FXN, HFE [52], HPX, HAMP, HFE2 [53], and FTMT [54], only the G258S polymorphism in the TF gene showed a statistically significant association with PD [17], although the finding was not replicated in a subsequent study [55], and a haplot…”
Result

Research works printed but not linked: 2

BL Pierce, 2011, Power and instrument strength requirements for Mendelian randomization studies using multiple genetic variants, Int J Epidemiol, 40, 740, 10.1093/ije/dyq151 · DOI
JL Fleiss, 1993, The statistical basis of meta-analysis, Stat Methods Med Res, 2, 121, 10.1177/096228029300200202 · DOI

Sorted by citations

Mendelian randomization: genetic anchors for causal inference in epidemiological studies
Davey Smith, G., & Hemani, G. (2014) · Human Molecular Genetics · doi:10.1093/hmg/ddu328 · Cited by 4,677
“Biomarkers CRP Coronary heart disease Observational association between CRP and coronary heart disease is a result of confounding and/or reverse causation (18) Serum iron Parkinson’s disease Higher serum iron levels lower the risk of Parkinson’s disease (19) Uric acid Coronary heart disease Observational association b…”
Background
The role of iron in brain ageing and neurodegenerative disorders
Ward, R. J., Zucca, F. A., Duyn, J. H., Crichton, R. R., & Zecca, L. (2014) · The Lancet Neurology · doi:10.1016/s1474-4422(14)70117-6 · Cited by 1,819
Detection and interpretation of shared genetic influences on 42 human traits
Pickrell, J. K., Berisa, T., Liu, J. Z., Ségurel, L., Tung, J. Y., & Hinds, D. A. (2016) · Nature Genetics · doi:10.1038/ng.3570 · Cited by 1,151
Mendelian randomization studies: a review of the approaches used and the quality of reporting
Boef, A. G. C., Dekkers, O. M., & le Cessie, S. (2015) · International Journal of Epidemiology · doi:10.1093/ije/dyv071 · Cited by 610
“One of the reviewed MR studies mentioned that the Wald-type estimator used to estimate an odds ratio was an approximate method.(169) The properties and limitations of these IV methods used to estimate a causal odds ratio deserve more attention in the Mendelian randomization studies in which they are used.”
Method
Iron neurochemistry in Alzheimer's disease and Parkinson's disease: targets for therapeutics
Belaidi, A. A., & Bush, A. I. (2015) · Journal of Neurochemistry · doi:10.1111/jnc.13425 · Cited by 594
“have been also proposed as a possible marker for PD in a large Mendelian randomization study (Pichler et al. 2013).”
Background

See all 173

Authors: Pichler, I., Del Greco M., F., Gögele, M., Lill, C. M., Bertram, L., Do, C. B., Eriksson, N., Foroud, T., Myers, R. H., PD GWAS Consortium, Nalls, M., Keller, M. F., International Parkinson's Disease Genomics Consortium, Wellcome Trust Case Control Consortium 2, Benyamin, B., Whitfield, J. B., Genetics of Iron Status Consortium, Pramstaller, P. P., Hicks, A. A., Thompson, J. R., & Minelli, C.
Affiliations: Eurac Research (IT)
Imperial College London (GB)
Johannes Gutenberg University Mainz (DE)
Max Planck Institute for Molecular Genetics (DE)
23andMe (United States) (US)
Indiana University School of Medicine (US)
Boston University (US)
National Institutes of Health (US)
The University of Queensland (AU)
QIMR Berghofer Medical Research Institute (AU)
Ospedale di Bolzano (IT)
University of Leicester (GB)
Corresponding author: Pichler, Irene
Minelli, Cosetta
ORCID: Pichler, Irene
Gögele, Martin
Lill, Christina M.
Bertram, Lars
Foroud, Tatiana
Myers, Richard H.
Keller, Margaux F.
Benyamin, Beben
Whitfield, John B.
Pramstaller, Peter P.
Hicks, Andrew A.
Minelli, Cosetta
Venue: PLoS Medicine
Publisher: Public Library of Science (PLoS)
Published: 2013-06-04
Volume: 10
Issue: 6
Pages: e1001462
ISSN: 1549-1277 (ISSN-L)
1549-1676
DOI: 10.1371/journal.pmed.1001462
PMC: PMC3672214
OpenAlex: W2169823945
Cited by: 173
References: 81
Citations by year: 2026: 2 · 2025: 5 · 2024: 11 · 2023: 9 · 2022: 14 · 2021: 27 · 2020: 13 · 2019: 16 · 2018: 10 · 2017: 14 · 2016: 18 · 2015: 17 · 2014: 15 · 2013: 2
FWCI: 11.01
Type: journal article
Language: en
Update notices: correction (2013-06-10)
Open access: gold
doi.org
Licence: cc-by
creativecommons.org/licenses/by/4.0/ (unspecified)
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Funders: U.S. Department of Defense (W81XWH, Z01-AG000949-02, Z01-ES101986, W81XWH0920128)
U.S. Department of Health and Human Services (W81XWH-09-2-0128, Z01-ES101986, RR024992, Z01‐AG000949‐02)
Michael J. Fox Foundation for Parkinson's Research (Z01-ES101986, W81XWH-09-2-0128, Z01-AG000949-02)
Susan G. Komen for the Cure
American Association for the Advancement of Science
Biogen
American Parkinson Disease Association
Cure Alzheimer's Fund
University of Rochester
University of Dundee
Queen Mary University of London
South London and Maudsley NHS Foundation Trust
Prize4Life
London School of Hygiene and Tropical Medicine
National Alliance for Research on Schizophrenia and Depression
Wellcome Trust (WT089698, 083948/Z/07/Z, WTCCC2, 090532, WTCCC1, NS057105, 083948, WT089698/Z/09/Z)
University Hospitals Birmingham NHS Foundation Trust
National Institute for Health and Care Research (NF-SI-0507-10376)
Parkinson's UK (F-1202, G0909, J-0901, J‐0804)
Imperial College London
King's College London
University College London
University of Oxford
European Commission (230596)
Cardiff University
University of Aberdeen
Trinity College Dublin
Agence Nationale de la Recherche
Institut National de la Santé et de la Recherche Médicale
Universiteit Leiden
Radboud Universiteit
Vrije Universiteit Amsterdam
Bundesministerium für Bildung und Forschung (01GR0468, 01GS08134, 01EW0908)
Centre National de la Recherche Scientifique
Leids Universitair Medisch Centrum
Deutsches Zentrum für Neurodegenerative Erkrankungen
Tartu Ülikool
Hersenstichting
Moorfields Eye Hospital NHS Foundation Trust
Provincia autonoma di Bolzano - Alto Adige
National Institutes of Health (1z01es101986-03, 5r44hg006981-03, W81XWH, UL1TR000448, W81XWH-09-2-0128, Z01‐AG000949‐02, Z01-ES101986, RR024992, NS057105, Z01-AG000949)
EMD Serono
Fidelity Biosciences
Medical Research Council (MR/K01417X/1, G0700943, WT089698)
Cambridge Institute for Medical Research, University of Cambridge
Erasmus Universitair Medisch Centrum Rotterdam
Diamantina Institute, University of Queensland
National Institute on Aging (Z01‐ES101986, W81XWH-09-2-0128, K24AG000949, Z01AG000949)
National Human Genome Research Institute (R44-HG006981)
National Institute of Neurological Disorders and Stroke (P30NS057105, NS057105, R01NS076843, P50NS071674)
National Institute of Environmental Health Sciences (Z01-ES 101986)
National Center for Research Resources (RR-024992, UL1RR024992)
NIH Clinical Center
National Center for Advancing Translational Sciences
Topics: Health Sciences › Medicine › Clinical Neurology › Parkinson's Disease Mechanisms and Treatments
Health Sciences › Medicine › Hematology › Iron Metabolism and Disorders
Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
Keywords: Parkinson's disease, serum iron, iron levels, disease risk, HFE gene, TMPRSS6, genetic instruments, causal effects, protective effect, biomarkers
MeSH terms: Humans, Iron, Parkinson Disease, Risk Factors, Genetic Predisposition to Disease, Genetic Association Studies, Mendelian Randomization Analysis

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Serum Iron Levels and the Risk of Parkinson Disease: A Mendelian Randomization Study

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