Trial reportBMC neurology2015
Ceruloplasmin activity and iron chelation treatment of patients with Parkinson's disease.
Trial report in BMC neurology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT00943748 (Efficacy and Safety of the Iron Chelator Deferiprone on Iron Overload in the Brain in Parkinson's Disease), which is not on this map. Cited by 52 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Efficacy and Safety of the Iron Chelator Deferiprone on Iron Overload in the Brain in Parkinson's Disease
Who cites it
52 citing papers in PubMed, 100 citations in OpenAlex.
- Programmed cell death pathways in huntington's disease: spotlight on ferroptosis and pyroptosis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026Review
- Ferroptosis inhibition protects against α-synuclein-related neuronal cell death.Cell death & disease · 2025Article
- Restless legs syndrome in Parkinson's disease: epidemiology, pathogenetic overlaps, and clinical management.Journal of neurology · 2025Review
- Epigenetic regulation of iron metabolism and ferroptosis in Parkinson's disease: Identifying novel epigenetic targets.Acta pharmacologica Sinica · 2025Review
- Homeostasis and metabolism of iron and other metal ions in neurodegenerative diseases.Signal transduction and targeted therapy · 2025Review
- Ferroptosis in central nervous system injuries: molecular mechanisms, diagnostic approaches, and therapeutic strategies.Frontiers in cellular neuroscience · 2025Review
- Uncovering Potential Biomarkers and Constructing a Prediction Model Associated with Iron Metabolism in Parkinson's Disease.Neuropsychiatric disease and treatment · 2025Article
- Small Molecules, α-Synuclein Pathology, and the Search for Effective Treatments in Parkinson's Disease.International journal of molecular sciences · 2024Review
- The involvement of α-synucleinopathy in the disruption of microglial homeostasis contributes to the pathogenesis of Parkinson's disease.Cell communication and signaling : CCS · 2024Review
- Mapping the Research of Ferroptosis in Parkinson's Disease from 2013 to 2023: A Scientometric Review.Drug design, development and therapy · 2024Review
- Research progress on ferroptosis in the pathogenesis and treatment of neurodegenerative diseases.Frontiers in cellular neuroscience · 2024Review
- The Construction and Validation of a Novel Ferroptosis-Related Gene Signature in Parkinson's Disease.International journal of molecular sciences · 2023Article
- Ferroptosis and Neurodegenerative Diseases: Insights into the Regulatory Roles of SLC7A11.Cellular and molecular neurobiology · 2023Review
- Inhibition of ACSL4 Alleviates Parkinsonism Phenotypes by Reduction of Lipid Reactive Oxygen Species.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023Article
- Induction Mechanism of Ferroptosis, Necroptosis, and Pyroptosis: A Novel Therapeutic Target in Nervous System Diseases.International journal of molecular sciences · 2023Review
- What Do Randomized Controlled Trials Inform Us About Potential Disease-Modifying Strategies for Parkinson's Disease?Neuromolecular medicine · 2023Review
- On the Chemical and Biological Characteristics of Multifunctional Compounds for the Treatment of Parkinson's Disease.Antioxidants (Basel, Switzerland) · 2023Review
- 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
- Review
- Dynamics of Nigral Iron Accumulation in Parkinson's Disease: From Diagnosis to Late Stage.Movement disorders : official journal of the Movement Disorder Society · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGrowing body of evidence suggests that Parkinson's disease (PD) is associated with oxidative damage via iron accumulation in the substantia nigra (SN). Low ceruloplasmin (CP)-ferroxidase activity has been identified in the SN and the cerebrospinal fluid (CSF) of patients with PD. The iron chelator, deferiprone, reduces the abnormally high levels of iron in the SN. In order to determine CP's involvement in iron accumulation in SN and PD progression, we aim to compare the ability of iron chelation treatment to reducing both SN iron levels and motor handicap in PD patients according to the level of ceruloplasmin activity.
methodsWe used a moderate chelation protocol with deferiprone (DFP) based on a, 6-month delayed-start paradigm, randomized placebo controlled clinical trial in 40 PD patients. CP-ferroxidase activity was determined in blood and CSF together with the D544E gene polymorphism (rs701753). Iron levels were determined by R2* MRI sequence and the motor handicap by the UPDRS motor score.
resultsAfter 6 to 12 months of DFP treatment, greater reductions in SN iron levels and UPDRS motor scores were obtained in patients with higher serum and CSF levels of CP-ferroxidase activity. After 6 months of DFP treatment, the AT genotype group displayed greater reduction of iron level in the SN with greater CSF and serum levels of CP activity than the AA genotype group.
conclusionAlthough most of the DFP-treated patients displayed clinical and radiological improvements, those with the lower CP activity appeared to respond better to iron chelation. Larger RCTs are now needed to establish whether pharmacological modulation of CP activity could be an innovative neuroprotective strategy in PD.
trial registrationFAIR-PARK study (ClinicalTrials.gov reference: NCT00943748 ; French national reference number: 2008-006842-25). This study was approved by the French Drug Agency (ANSM) and the local institutional review board ("Comité de Protection des Personnes of Lille").
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.