ReviewFrontiers in aging neuroscience2022
Iron Dyshomeostasis and Ferroptosis: A New Alzheimer's Disease Hypothesis?
Review in Frontiers in aging neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 papers.
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Who cites it
102 citing papers in PubMed, 156 citations in OpenAlex.
- Trace Elements Dyshomeostasis and Toxic Metals Neurotoxicity in Neurodegenerative Diseases.Biological trace element research · 2026Review
- Differential Effects of Cannabidiol and Cannabigerol on Cognition, Neuroinflammation, and Blood-Brain Barrier Integrity in a Rat Model of Iron Overload.Neurotoxicity research · 2026Article
- Metallothionein and neurodegenerative diseases.Neural regeneration research · 2026Article
- Ferroptosis and aging: Inducing and catalyzing neurodegenerative diseases.Neural regeneration research · 2026Article
- Integrative role of orexigenic peptides in neuroprotection and neurodegenerative disease modulation.Bioscience reports · 2026Review
- The iron-energy metabolism axis in Alzheimer's pathogenesis: from mechanisms to interventions.Cell death discovery · 2026Review
- Pulmonary neuroendocrine cell-derived exosomes regulate iron homeostasis and oxidative stress in lung neurons.Science advances · 2026Article
- Unraveling the molecular mechanisms of aluminium chloride-induced Alzheimer's disease.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026Review
- Longitudinal analysis of hippocampal subfield atrophy and network centrality associated with cognitive decline in Alzheimer's disease progression.Medical physics · 2026Article
- The brain and heart-axis in neurodegeneration and cardiovascular disease.Journal of neural transmission (Vienna, Austria : 1996) · 2026Review
- Upregulation of SLC38A2 by melatonin attenuates hippocampal ferroptosis in Alzheimer's disease.Alzheimer's research & therapy · 2026Article
- PRDX6 as a Ferroptosis-Related Hub Gene in the Entorhinal Cortex of Alzheimer's Disease: A Multidimensional Bioinformatics and Experimental Validation Study.Journal of molecular neuroscience : MN · 2026Article
- β-Alanine Is an Unexploited Neurotransmitter in the Pathogenesis and Treatment of Alzheimer's Disease.NeuroSci · 2026Review
- Metabolic cell death networks in Alzheimer's disease: mechanistic links and therapeutic perspectives of ferroptosis, cuproptosis, and disulfidptosis.Frontiers in cell and developmental biology · 2026Review
- Ferroptosis in microglial activation: a systematic review and multidata comparison.Brain communications · 2026Review
- Autophagy-lysosomal pathway in neurodegeneration.Molecular neurodegeneration advances · 2026Review
- Development and translation of biodegradable metal stents: from heart to brain.Regenerative biomaterials · 2026Review
- PPARG as a central regulator of ferroptosis in Alzheimer's disease: integrated transcriptomic, single-cell, and experimental evidence.Frontiers in aging neuroscience · 2026Article
- Ferroptosis-immune crosstalk in CNS diseases: mechanisms and translational insights.Frontiers in immunology · 2026Review
- Metal ion dyshomeostasis in neurological disorders: from pathological mechanisms to targeted neuroprotective and regenerative strategies.Frontiers in pharmacology · 2026Review
42 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Iron plays a crucial role in many physiological processes of the human body, but iron is continuously deposited in the brain as we age. Early studies found iron overload is directly proportional to cognitive decline in Alzheimer's disease (AD). Amyloid precursor protein (APP) and tau protein, both of which are related to the AD pathogenesis, are associated with brain iron metabolism. A variety of iron metabolism-related proteins have been found to be abnormally expressed in the brains of AD patients and mouse models, resulting in iron deposition and promoting AD progression. Amyloid β (Aβ) and hyperphosphorylated tau, two pathological hallmarks of AD, can also promote iron deposition in the brain, forming a vicious cycle of AD development-iron deposition. Iron deposition and the subsequent ferroptosis has been found to be a potential mechanism underlying neuronal loss in many neurodegenerative diseases. Iron chelators, antioxidants and hepcidin were found useful for treating AD, which represents an important direction for AD treatment research and drug development in the future. The review explored the deep connection between iron dysregulation and AD pathogenesis, discussed the potential of new hypothesis related to iron dyshomeostasis and ferroptosis, and summarized the therapeutics capable of targeting iron, with the expectation to draw more attention of iron dysregulation and corresponding drug development.
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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.