ReviewNeurochemical research2024
Epigenetic Mechanisms of Aluminum-Induced Neurotoxicity and Alzheimer's Disease: A Focus on Non-Coding RNAs.
Review in Neurochemical research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed.
- The neuroprotective potential of thymoquinone and intermittent fasting on aluminum chloride-induced Alzheimer's disease like model in rat hippocampus: insights into neurogenesis and autophagy.Journal of molecular histology · 2026Article
- Dietary Aluminium Exposure and Human Health: Sources, Bioavailability, Toxicokinetics, and Health Risk Assessment.Nutrients · 2026Review
- Serum Trace-Element Profiles and Exploratory Composite Indices in Multiple System Atrophy: A Case-Control Study.Diagnostics (Basel, Switzerland) · 2026Article
- MicroRNA-Mediated Regulation of Brain Aging Hallmarks: Implications for Neurodegeneration and Neural Recovery.Brain and behavior · 2026Review
- Multifaceted roles of miR‑124 in cancer: Molecular mechanisms and clinical prospects (Review).International journal of oncology · 2026Review
- Aluminum Chloride-Driven Neurodegeneration: Interlinking Redox Imbalance, Inflammation Cascade, and Excitotoxic Damage Across Molecular and Behavioral Domains.Molecular neurobiology · 2026Review
- Mechanisms of neurotoxicity of fluoride or aluminum: implications for neurodegenerative disease risk.Current research in toxicology · 2026Review
- The Role of Epigenetics in Manganese Neurotoxicity: An Update with a Focus on Non-Coding RNAs and Histone Modifications.Neurochemical research · 2025Review
- Agonism of MTNeurochemical research · 2025Article
- The Neuroprotective Impact of Agomelatine in Preserving Brain Tissue Molecular Structure Against Alzheimer's Disease Etiology.Neurochemical research · 2025Article
- Elevated Expression of STAT6, ERG, and miR-647 Expression as Predictive Biomarkers for Prostate Cancer.International journal of general medicine · 2025Article
- Repositioning Canagliflozin for Mitigation of Aluminium Chloride-Induced Alzheimer's Disease: Involvement of TXNIP/NLRP3 Inflammasome Axis, Mitochondrial Dysfunction, and SIRT1/HMGB1 Signalling.Medicina (Kaunas, Lithuania) · 2024Article
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Abstract
Aluminum (Al) is known to induce neurotoxic effects, potentially contributing to Alzheimer's disease (AD) pathogenesis. Recent studies suggest that epigenetic modification may contribute to Al neurotoxicity, although the mechanisms are still debatable. Therefore, the objective of the present study was to summarize existing data on the involvement of epigenetic mechanisms in Al-induced neurotoxicity, especially AD-type pathology. Existing data demonstrate that Al exposure induces disruption in DNA methylation, histone modifications, and non-coding RNA expression in brains. Alterations in DNA methylation following Al exposure were shown to be mediated by changes in expression and activity of DNA methyltransferases (DNMTs) and ten-eleven translocation proteins (TETs). Al exposure was shown to reduce histone acetylation by up-regulating expression of histone deacetylases (HDACs) and impair histone methylation, ultimately contributing to down-regulation of brain-derived neurotrophic factor (BDNF) expression and activation of nuclear factor κB (NF-κB) signaling. Neurotoxic effects of Al exposure were also associated with aberrant expression of non-coding RNAs, especially microRNAs (miR). Al-induced patterns of miR expression were involved in development of AD-type pathology by increasing amyloid β (Aβ) production through up-regulation of Aβ precursor protein (APP) and β secretase (BACE1) expression (down-regulation of miR-29a/b, miR-101, miR-124, and Let-7c expression), increasing in neuroinflammation through NF-κB signaling (up-regulation of miR-9, miR-125b, miR-128, and 146a), as well as modulating other signaling pathways. Furthermore, reduced global DNA methylation, altered histone modification, and aberrant miRNA expression were associated with cognitive decline in Al-exposed subjects. However, further studies are required to evaluate the contribution of epigenetic mechanisms to Al-induced neurotoxicity and/or AD development.
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