ReviewOxidative medicine and cellular longevity2018
Unraveling the Burden of Iron in Neurodegeneration: Intersections with Amyloid Beta Peptide Pathology.
Review in Oxidative medicine and cellular longevity, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis 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
28 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Molecular mechanisms of programmed cell death in methamphetamine-induced neuronal damage.Frontiers in pharmacology · 2022Pooled it
- Lycium barbarum glycopeptide reduces brain damage following ischemic stroke by inhibiting ferroptosis and oxidation.Neural regeneration research · 2026Article
- Wnt/β-catenin Pathway Activation Reverses Tau Hyperphosphorylation and β-Amyloid Accumulation Induced by Combined Manganese and Iron Exposure in PC12 Cells.Biological trace element research · 2026Article
- Reevaluating the role of amyloidFrontiers in neurology · 2025Review
- The Impact of the Combined Effect of Inhalation Anesthetics and Iron Dextran on Rats' Systemic Toxicity.International journal of molecular sciences · 2024Article
- Fluid biomarkers in cerebral amyloid angiopathy.Frontiers in neuroscience · 2024Review
- Global Research Trends and Hotspots for Ferroptosis, Necroptosis, and Pyroptosis in Alzheimer's Disease from the Past to 2023: A Combined Bibliometric Review.Journal of Alzheimer's disease reports · 2024Review
- Astaxanthin attenuates cognitive deficits in Alzheimer's disease models by reducing oxidative stress via the SIRT1/PGC-1α signaling pathway.Cell & bioscience · 2023Article
- Inflammation, Dopaminergic Brain and Bilirubin.International journal of molecular sciences · 2023Review
- Intranasal Lipid Nanoparticles Containing Bioactive Compounds Obtained from Marine Sources to Manage Neurodegenerative Diseases.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Iron overload and chelation modulates bisretinoid levels in the retina.Frontiers in ophthalmology · 2023Article
- FTH1- and SAT1-Induced Astrocytic Ferroptosis Is Involved in Alzheimer's Disease: Evidence from Single-Cell Transcriptomic Analysis.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Proteomic analysis of human hippocampal subfields provides new insights into the pathogenesis of Alzheimer's disease and the role of glial cells.Brain pathology (Zurich, Switzerland) · 2022Article
- A DistinctCells · 2022Article
- Selected Natural Products in Neuroprotective Strategies for Alzheimer's Disease-A Non-Systematic Review.International journal of molecular sciences · 2022Review
- Redox-Active Metal Ions and Amyloid-Degrading Enzymes in Alzheimer's Disease.International journal of molecular sciences · 2021Review
- Gossypitrin, A Naturally Occurring Flavonoid, Attenuates Iron-Induced Neuronal and Mitochondrial Damage.Molecules (Basel, Switzerland) · 2021Article
- Insights into the Roles of the Sideroflexins/SLC56 Family in Iron Homeostasis and Iron-Sulfur Biogenesis.Biomedicines · 2021Review
- Up-regulation of hypoxia-inducible factor antisense as a novel approach to treat ovarian cancer.Theranostics · 2020Article
- Anti-inflammatory and Neuroprotective Agents in Clinical Trials for CNS Disease and Injury: Where Do We Go From Here?Frontiers in immunology · 2020Review
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Iron overload is a hallmark of many neurodegenerative processes such as Alzheimer's, Parkinson's, and Huntington's diseases. Unbound iron accumulated as a consequence of brain aging is highly reactive with water and oxygen and produces reactive oxygen species (ROS) or free radicals. ROS are toxic compounds able to damage cell membranes, DNA, and mitochondria. Which are the mechanisms involved in neuronal iron homeostasis and in neuronal response to iron-induced oxidative stress constitutes a cutting-edge topic in metalloneurobiology. Increasing our knowledge about the underlying mechanisms that operate in iron accumulation and their consequences would shed light on the comprehension of the molecular events that participate in the pathophysiology of the abovementioned neurodegenerative diseases. In this review, current evidences about iron accumulation in the brain, the signaling mechanisms triggered by metal overload, as well as the interaction between amyloid
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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.