ReviewOxidative medicine and cellular longevity2013
Metal dyshomeostasis and inflammation in Alzheimer's and Parkinson's diseases: possible impact of environmental exposures.
Review in Oxidative medicine and cellular longevity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 1 of them a synthesis that pooled it.
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Who cites it
67 citing papers in PubMed, 1 synthesis or guideline pooled it, 148 citations in OpenAlex.
- Transcriptomics Meta-Analysis Reveals Phagosome and Innate Immune System Dysfunction as Potential Mechanisms in the Cortex of Alzheimer's Disease Mouse Strains.Journal of molecular neuroscience : MN · 2023Pooled it
- Pulmonary neuroendocrine cell-derived exosomes regulate iron homeostasis and oxidative stress in lung neurons.Science advances · 2026Article
- Prolonged duration induces divergent transcriptomic responses to manganese, distinct from concentration effects, in an SH-SY5Y neurotoxicity model.Neurotoxicology · 2026Article
- Cell type transcriptomic modules reveal shared molecular mechanisms in Alzheimer's and Parkinson's disease.GigaScience · 2026Article
- From dysbiosis to dysfunction: specific gut microbes and metabolites in the pathogenesis of Parkinson's disease.Sustainable microbiology · 2026Review
- The Potential of Coenzyme Q10 in Alzheimer's Disease: Reducing IL-17 Induced Inflammation and Oxidative Stress for Neuroprotection.Current drug research reviews · 2026Review
- Oxidative stress indicators mediated the association of dietary copper intake with low muscle mass: a cross-sectional study.NPJ science of food · 2025Article
- Comparison of Morphological Signs of Neurodegenerative Changes and Expression of Neuroprotective Factors in Adult and Aged Wistar Rats in AlClBulletin of experimental biology and medicine · 2025Article
- Targeting Metal Imbalance and Oxidative Stress in Alzheimer's Disease with Novel Multifunctional Compounds.Molecules (Basel, Switzerland) · 2025Review
- Function and application of brain‑derived neurotrophic factor precursors (Review).International journal of molecular medicine · 2025Review
- Chronic Vanadium Exposure Promotes Aggregation of Alpha-Synuclein, Tau and Amyloid Beta in Mouse Brain.Journal of neurochemistry · 2025Article
- The Role of IL-17A in Mediating Inflammatory Responses and Progression of Neurodegenerative Diseases.International journal of molecular sciences · 2025Review
- Downregulation of Parahippocampal Copper Chaperone for Superoxide Dismutase in Alzheimer's Disease.Brain sciences · 2025Article
- Selenoproteins: Zoom-In to Their Metal-Binding Properties in Neurodegenerative Diseases.International journal of molecular sciences · 2025Review
- Urinary Metal Levels, Cognitive Test Performance, and Dementia in the Multi-Ethnic Study of Atherosclerosis.JAMA network open · 2024Article
- Article
- Protective role of hesperetin in Drosophila melanogaster model of ferrous sulphate-induced toxicity.BMC pharmacology & toxicology · 2024Article
- The potential significance of hepcidin evaluation in progressive supranuclear palsy.Brain and behavior · 2024Article
- Article
- Advancements in Genetic and Biochemical Insights: Unraveling the Etiopathogenesis of Neurodegeneration in Parkinson's Disease.Biomolecules · 2024Review
7 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A dysregulated metal homeostasis is associated with both Alzheimer's (AD) and Parkinson's (PD) diseases; AD patients have decreased cortex and elevated serum copper levels along with extracellular amyloid-beta plaques containing copper, iron, and zinc. For AD, a putative hepcidin-mediated lowering of cortex copper mechanism is suggested. An age-related mild chronic inflammation and/or elevated intracellular iron can trigger hepcidin production followed by its binding to ferroportin which is the only neuronal iron exporter, thereby subjecting it to lysosomal degradation. Subsequently raised neuronal iron levels can induce translation of the ferroportin assisting and copper binding amyloid precursor protein (APP); constitutive APP transmembrane passage lowers the copper pool which is important for many enzymes. Using in silico gene expression analyses, we here show significantly decreased expression of copper-dependent enzymes in AD brain and metallothioneins were upregulated in both diseases. Although few AD exposure risk factors are known, AD-related tauopathies can result from cyanobacterial microcystin and β-methylamino-L-alanine (BMAA) intake. Several environmental exposures may represent risk factors for PD; for this disease neurodegeneration is likely to involve mitochondrial dysfunction, microglial activation, and neuroinflammation. Administration of metal chelators and anti-inflammatory agents could affect disease outcomes.
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