ArticleNeurobiology of disease2014
Pooled analysis of iron-related genes in Parkinson's disease: association with transferrin.
Article in Neurobiology of disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 84 citations in OpenAlex.
- Reimagining the contribution of iron in Parkinson's disease.Neurobiology of disease · 2026Review
- HFE genotype influences substantia nigra iron accumulation and Parkinson's disease progression.medRxiv : the preprint server for health sciences · 2026Article
- When Pathways Converge: Iron, Lipid Peroxidation, and α-Synuclein in Ferroptosis-Driven Dopaminergic Neurodegeneration.Journal of neurochemistry · 2026Review
- Autophagy-lysosomal pathway in neurodegeneration.Molecular neurodegeneration advances · 2026Review
- A novel expectation-maximization approach to infer general diploid selection from time-series genetic data.PLoS genetics · 2025Article
- A novel expectation-maximization approach to infer general diploid selection from time-series genetic data.bioRxiv : the preprint server for biology · 2025Article
- Ferroptosis: a novel pathogenesis and therapeutic strategies for Parkinson disease: A review.Medicine · 2025Review
- Iron homeostasis and ferroptosis in human diseases: mechanisms and therapeutic prospects.Signal transduction and targeted therapy · 2024Review
- Ferroptosis-A Shared Mechanism for Parkinson's Disease and Type 2 Diabetes.International journal of molecular sciences · 2024Review
- Quantitative susceptibility mapping of subcortical iron deposition in Parkinson disease and multiple system atrophy: clinical correlations and diagnostic implications.Quantitative imaging in medicine and surgery · 2024Article
- Ferritinophagy: A novel insight into the double-edged sword in ferritinophagy-ferroptosis axis and human diseases.Cell proliferation · 2024Review
- HMGB1 Mediates Inflammation-Induced DMT1 Increase and Dopaminergic Neurodegeneration in the Early Stage of Parkinsonism.Molecular neurobiology · 2024Article
- Research progress on ferroptosis in the pathogenesis and treatment of neurodegenerative diseases.Frontiers in cellular neuroscience · 2024Review
- Pharmacological Inhibition of Ferroptosis as a Therapeutic Target for Neurodegenerative Diseases and Strokes.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Review
- In situ continuous Dopa supply by responsive artificial enzyme for the treatment of Parkinson's disease.Nature communications · 2023Article
- Unscrambling the Role of Redox-Active Biometals in Dopaminergic Neuronal Death and Promising Metal Chelation-Based Therapy for Parkinson's Disease.International journal of molecular sciences · 2023Review
- Article
- Molecular Mechanisms of Autophagy in Cancer Development, Progression, and Therapy.Biomedicines · 2022Review
- Increased Transferrin Sialylation Predicts Phenoconversion in Isolated REM Sleep Behavior Disorder.Movement disorders : official journal of the Movement Disorder Society · 2022Article
- Ferroptosis and Its Potential Role in the Nervous System Diseases.Journal of inflammation research · 2022Review
Corrections and comments
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Authors and funding
11 authors at 7 institutions in 3 countries.
Funding
Abstract
Pathologic features of Parkinson's disease (PD) include death of dopaminergic neurons in the substantia nigra, presence of α-synuclein containing Lewy bodies, and iron accumulation in PD-related brain regions. The observed iron accumulation may be contributing to PD etiology but it also may be a byproduct of cell death or cellular dysfunction. To elucidate the possible role of iron accumulation in PD, we investigated genetic variation in 16 genes related to iron homeostasis in three case-control studies from the United States, Australia, and France. After screening 90 haplotype tagging single nucleotide polymorphisms (SNPs) within the genes of interest in the US study population, we investigated the five most promising gene regions in two additional independent case-control studies. For the pooled data set (1289 cases, 1391 controls) we observed a protective association (OR=0.83, 95% CI: 0.71-0.96) between PD and a haplotype composed of the A allele at rs1880669 and the T allele at rs1049296 in transferrin (TF; GeneID: 7018). Additionally, we observed a suggestive protective association (OR=0.87, 95% CI: 0.74-1.02) between PD and a haplotype composed of the G allele at rs10247962 and the A allele at rs4434553 in transferrin receptor 2 (TFR2; GeneID: 7036). We observed no associations in our pooled sample for haplotypes in SLC40A1, CYB561, or HFE. Taken together with previous findings in model systems, our results suggest that TF or a TF-TFR2 complex may have a role in the etiology of PD, possibly through iron misregulation or mitochondrial dysfunction within dopaminergic neurons.
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