ReviewCurrent neuropharmacology2019
Does Ceruloplasmin Defend Against Neurodegenerative Diseases?
Review in Current neuropharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 3 of them syntheses that pooled it.
What it found
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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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
59 citing papers in PubMed, 3 syntheses or guidelines pooled it, 97 citations in OpenAlex.
- Pooled it
- The Role of Selected Trace Elements in Oxidoreductive Homeostasis in Patients with Thyroid Diseases.International journal of molecular sciences · 2023Pooled it
- A novel ceruloplasmin mutation identified in a Chinese patient and clinical spectrum of aceruloplasminemia patients.Metabolic brain disease · 2021Pooled it
- A diagnostic dilemma in a child with Wilson's disease.Pediatric nephrology (Berlin, Germany) · 2026Article
- Review
- Serum Proteomics of Multiple Menstrual Symptoms in Female Athletes: A Pilot Study.FASEB bioAdvances · 2026Article
- Copper Dyshomeostasis Affects α-Synuclein Clearance Mechanisms in Parkinson's Disease: Insights from In Vitro Models and Translational Evidence.International journal of molecular sciences · 2026Review
- Unraveling genotype-phenotype relationships in hereditary hemochromatosis through integrated biobank data analysis.BMC genomics · 2026Article
- The Molecular Pathology of Non-Malignant Haematological Disease.British journal of biomedical science · 2026Review
- Proteomics analysis of aqueous and vitreous humor in uveitis: a systematic literature review.Clinical proteomics · 2025Review
- Machine learning identifies lactate metabolism biomarkers and deciphers immune infiltration landscapes in Parkinson's disease.Scientific reports · 2025Article
- TDMQ20 as A Drug Candidate for Wilson's Disease: Comparison with D-Penicillamine, Trientine, and Tetrathiomolybdate In Vitro and In Mice.Pharmaceutics · 2025Article
- Sex- and age- differences in the expression of critical blood-brain barrier regulators: a physiological context.Biology of sex differences · 2025Article
- [Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025Article
- Plasma Proteome Profiling Reveals Inflammation Markers and Tafamidis Effects in V30M Transthyretin Polyneuropathy.International journal of molecular sciences · 2025Article
- Ferroptosis: a novel pathogenesis and therapeutic strategies for Parkinson disease: A review.Medicine · 2025Review
- Relationship between reduced serum ceruloplasmin levels and executive dysfunction in hospitalized schizophrenia patients.Frontiers in psychiatry · 2025Article
- Iron responsive elements mRNA regulate Alzheimer's amyloid precursor protein translation through iron sensing.Frontiers in aging neuroscience · 2025Review
- A Novel Mutation Related to Aceruloplasminemia with Mild Clinical Findings: A Case Report.Reports (MDPI) · 2024Article
- The Role of Selected Elements in Oxidative Stress Protection: Key to Healthy Fertility and Reproduction.International journal of molecular sciences · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ceruloplasmin (CP) is the major copper transport protein in plasma, mainly produced by the liver. Glycosylphosphatidylinositol-linked CP (GPI-CP) is the predominant form expressed in astrocytes of the brain. A growing body of evidence has demonstrated that CP is an essential protein in the body with multiple functions such as regulating the homeostasis of copper and iron ions, ferroxidase activity, oxidizing organic amines, and preventing the formation of free radicals. In addition, as an acute-phase protein, CP is induced during inflammation and infection. The fact that patients with genetic disorder aceruloplasminemia do not suffer from tissue copper deficiency, but rather from disruptions in iron metabolism shows essential roles of CP in iron metabolism rather than copper. Furthermore, abnormal metabolism of metal ions and oxidative stress are found in other neurodegenerative diseases, such as Wilson's disease, Alzheimer's disease and Parkinson's disease. Brain iron accumulation and decreased activity of CP have been shown to be associated with neurodegeneration. We hypothesize that CP may play a protective role in neurodegenerative diseases. However, whether iron accumulation is a cause or a result of neurodegeneration remains unclear. Further research on molecular mechanisms is required before a consensus can be reached regarding a neuroprotective role for CP in neurodegeneration. This review article summarizes the main physiological functions of CP and the current knowledge of its role in neurodegenerative diseases.
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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.