ReviewFrontiers in pharmacology2014
The iron regulatory capability of the major protein participants in prevalent neurodegenerative disorders.
Review in Frontiers in pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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.
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Who cites it
22 citing papers in PubMed, 49 citations in OpenAlex.
- Gerstmann-Sträussler-Scheinker Disease Presenting as Late-Onset Slowly Progressive Spinocerebellar Ataxia, and Comparative Case Series with Neuropathology.Movement disorders clinical practice · 2024Article
- Synthesis, physicochemical characterization and neuroprotective evaluation of novel 1-hydroxypyrazin-2(1Dalton transactions (Cambridge, England : 2003) · 2022Article
- Interaction between Hemin and Prion Peptides: Binding, Oxidative Reactivity and Aggregation.International journal of molecular sciences · 2020Article
- Exploring the Use of Dimethyl Fumarate as Microglia Modulator for Neurodegenerative Diseases Treatment.Antioxidants (Basel, Switzerland) · 2020Review
- High Dietary Iron Disrupts Iron Homeostasis and Induces Amyloid-β and Phospho-τ Expression in the Hippocampus of Adult Wild-Type and APP/PS1 Transgenic Mice.The Journal of nutrition · 2019Article
- Iron Redox Chemistry and Implications in the Parkinson's Disease Brain.Oxidative medicine and cellular longevity · 2019Review
- Unraveling the Burden of Iron in Neurodegeneration: Intersections with Amyloid Beta Peptide Pathology.Oxidative medicine and cellular longevity · 2018Review
- Cardiac Light Chain Amyloidosis: The Role of Metal Ions in Oxidative Stress and Mitochondrial Damage.Antioxidants & redox signaling · 2017Article
- Post translational changes to α-synuclein control iron and dopamine trafficking; a concept for neuron vulnerability in Parkinson's disease.Molecular neurodegeneration · 2017Review
- Contributions to magnetic susceptibility of brain tissue.NMR in biomedicine · 2017Review
- Iron-Restricted Diet Affects Brain Ferritin Levels, Dopamine Metabolism and Cellular Prion Protein in a Region-Specific Manner.Frontiers in molecular neuroscience · 2017Article
- Bioavailable Trace Metals in Neurological Diseases.Current treatment options in neurology · 2016Review
- α-Synuclein Over-Expression Induces Increased Iron Accumulation and Redistribution in Iron-Exposed Neurons.Molecular neurobiology · 2016Article
- Role of iron in neurodegenerative diseases.Journal of neural transmission (Vienna, Austria : 1996) · 2016Review
- Iron Homeostasis in Health and Disease.International journal of molecular sciences · 2016Review
- Unified theory of Alzheimer's disease (UTAD): implications for prevention and curative therapy.Journal of molecular psychiatry · 2016Review
- Prion protein functions as a ferrireductase partner for ZIP14 and DMT1.Free radical biology & medicine · 2015Article
- Review
- The importance of iron in pathophysiologic conditions.Frontiers in pharmacology · 2015Article
- Uptake and metabolism of iron oxide nanoparticles in brain cells.Neurochemical research · 2014Review
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 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
As with most bioavailable transition metals, iron is essential for many metabolic processes required by the cell but when left unregulated is implicated as a potent source of reactive oxygen species. It is uncertain whether the brain's evident vulnerability to reactive species-induced oxidative stress is caused by a reduced capability in cellular response or an increased metabolic activity. Either way, dys-regulated iron levels appear to be involved in oxidative stress provoked neurodegeneration. As in peripheral iron management, cells within the central nervous system tightly regulate iron homeostasis via responsive expression of select proteins required for iron flux, transport and storage. Recently proteins directly implicated in the most prevalent neurodegenerative diseases, such as amyloid-β precursor protein, tau, α-synuclein, prion protein and huntingtin, have been connected to neuronal iron homeostatic control. This suggests that disrupted expression, processing, or location of these proteins may result in a failure of their cellular iron homeostatic roles and augment the common underlying susceptibility to neuronal oxidative damage that is triggered in neurodegenerative disease.
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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.