ArticlePloS one2011
Microarray analysis on human neuroblastoma cells exposed to aluminum, β(1-42)-amyloid or the β(1-42)-amyloid aluminum complex.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
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Who cites it
14 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Systematic review of potential health risks posed by pharmaceutical, occupational and consumer exposures to metallic and nanoscale aluminum, aluminum oxides, aluminum hydroxide and its soluble salts.Critical reviews in toxicology · 2014Pooled it
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- Roles of receptor-interacting protein kinase 1 in SH-SY5Y cells with beta amyloid-induced neurotoxicity.Journal of cellular and molecular medicine · 2022Article
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- Identification of Methylated Gene Biomarkers in Patients with Alzheimer's Disease Based on Machine Learning.BioMed research international · 2020Article
- Identification of the Role of miR-142-5p in Alzheimer's Disease by Comparative Bioinformatics and Cellular Analysis.Frontiers in molecular neuroscience · 2017Article
- Runx2 expression: A mesenchymal stem marker for cancer.Oncology letters · 2016Article
- Apoptosis in Alzheimer's disease: an understanding of the physiology, pathology and therapeutic avenues.Neurochemical research · 2014Review
- Gene expression and highly diluted molecules.Frontiers in pharmacology · 2014Article
- Aluminum-induced entropy in biological systems: implications for neurological disease.Journal of toxicology · 2014Review
- Robust selection of cancer survival signatures from high-throughput genomic data using two-fold subsampling.PloS one · 2014Article
- Identification of genes potentially regulated by human polynucleotide phosphorylase (hPNPase old-35) using melanoma as a model.PloS one · 2013Article
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundA typical pathological feature of Alzheimer's disease (AD) is the appearance in the brain of senile plaques made up of β-amyloid (Aβ) and neurofibrillary tangles. AD is also associated with an abnormal accumulation of some metal ions, and we have recently shown that one of these, aluminum (Al), plays a relevant role in affecting Aβ aggregation and neurotoxicity. METHODOLOGY: In this study, employing a microarray analysis of 35,129 genes, we investigated the effects induced by the exposure to the Aβ(1-42)-Al (Aβ-Al) complex on the gene expression profile of the neuronal-like cell line, SH-SY5Y. PRINCIPAL
findingsThe microarray assay indicated that, compared to Aβ or Al alone, exposure to Aβ-Al complex produced selective changes in gene expression. Some of the genes selectively over or underexpressed are directly related to AD. A further evaluation performed with Ingenuity Pathway analysis revealed that these genes are nodes of networks and pathways that are involved in the modulation of Ca(2+) homeostasis as well as in the regulation of glutamatergic transmission and synaptic plasticity. CONCLUSIONS AND SIGNIFICANCE: Aβ-Al appears to be largely involved in the molecular machinery that regulates neuronal as well as synaptic dysfunction and loss. Aβ-Al seems critical in modulating key AD-related pathways such as glutamatergic transmission, Ca(2+) homeostasis, oxidative stress, inflammation, and neuronal apoptosis.
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