ArticleJournal of Alzheimer's disease : JAD2013
Prion protein regulates iron transport by functioning as a ferrireductase.
Article in Journal of Alzheimer's disease : JAD, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 86 citations in OpenAlex.
- Beyond Neurodegeneration: White Matter Vacuolation as a Primary Myelin Defect.International journal of molecular sciences · 2026Review
- Exploring and Targeting the Connection of Iron and Copper Homeostasis to Neurodegenerative Diseases.MedComm · 2026Review
- Molecular Mechanisms of Iron Metabolism and Overload.Biomedicines · 2025Review
- Prion-induced ferroptosis is facilitated by RAC3.Nature communications · 2025Article
- The Underestimated Role of Iron in Frontotemporal Dementia: A Narrative Review.International journal of molecular sciences · 2024Review
- Gerstmann-Sträussler-Scheinker Disease Presenting as Late-Onset Slowly Progressive Spinocerebellar Ataxia, and Comparative Case Series with Neuropathology.Movement disorders clinical practice · 2024Article
- Dysregulation of iron homeostasis and ferroptosis in sevoflurane and isoflurane associated perioperative neurocognitive disorders.CNS neuroscience & therapeutics · 2024Review
- Bridging Retinal and Cerebral Neurodegeneration: A Focus on Crosslinks between Alzheimer-Perusini's Disease and Retinal Dystrophies.Biomedicines · 2023Review
- Cellular prion protein offers neuroprotection in astrocytes submitted to amyloid β oligomer toxicity.Molecular and cellular biochemistry · 2023Article
- Mitochondrial Regulation of Ferroptosis in Cancer Therapy.International journal of molecular sciences · 2023Review
- Review
- The Emerging Role of Ferroptosis in Liver Cancers.Life (Basel, Switzerland) · 2022Review
- New Players in Neuronal Iron Homeostasis: Insights from CRISPRi Studies.Antioxidants (Basel, Switzerland) · 2022Article
- Crosstalk of copper and zinc in the pathogenesis of vascular dementia.Journal of clinical biochemistry and nutrition · 2022Article
- Melatonin: Regulation of Prion Protein Phase Separation in Cancer Multidrug Resistance.Molecules (Basel, Switzerland) · 2022Review
- Iron Dyshomeostasis and Ferroptosis: A New Alzheimer's Disease Hypothesis?Frontiers in aging neuroscience · 2022Review
- β-Cleavage of the prion protein in the human eye: Implications for the spread of infectious prions and human ocular disorders.Experimental eye research · 2021Article
- Copper as a Collaborative Partner of Zinc-Induced Neurotoxicity in the Pathogenesis of Vascular Dementia.International journal of molecular sciences · 2021Review
- Harnessing the Physiological Functions of Cellular Prion Protein in the Kidneys: Applications for Treating Renal Diseases.Biomolecules · 2021Review
- Aging lens epithelium is susceptible to ferroptosis.Free radical biology & medicine · 2021Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Prion protein (PrPC) is implicated in the pathogenesis of prion disorders, but its normal function is unclear. We demonstrate that PrPC is a ferrireductase (FR), and its absence causes systemic iron deficiency in PrP knock-out mice (PrP-/-). When exposed to non-transferrin-bound (NTB) radioactive-iron (59FeCl3) by gastric-gavage, PrP-/- mice absorb significantly more 59Fe from the intestinal lumen relative to controls, indicating appropriate systemic response to the iron deficiency. Chronic exposure to excess dietary iron corrects this deficiency, but unlike wild-type (PrP+/+) controls that remain iron over-loaded, PrP-/- mice revert back to the iron deficient phenotype after 5 months of chase on normal diet. Bone marrow (BM) preparations of PrP-/- mice on normal diet show relatively less stainable iron, and this phenotype is only partially corrected by intraperitoneal administration of excess iron-dextran. Cultured PrP-/- BM-macrophages incorporate significantly less NTB-59Fe in the absence or presence of excess extracellular iron, indicating reduced uptake and/or storage of available iron in the absence of PrPC. When expressed in neuroblastoma cells, PrPC exhibits NAD(P)H-dependent cell-surface and intracellular FR activity that requires the copper-binding octa-peptide-repeat region and linkage to the plasma membrane for optimal function. Incorporation of NTB-59Fe by neuroblastoma cells correlates with FR activity of PrPC, implicating PrPC in cellular iron uptake and metabolism. These observations explain the correlation between PrPC expression and cellular iron levels, and the cause of iron imbalance in sporadic-Creutzfeldt-Jakob-disease brains where PrPC accumulates as insoluble aggregates.
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