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EnglishBackground: A typical pathological feature of Alzheimer’s disease (AD) is the appearance in the brain of senile plaques made up of b-amyloid (Ab) 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 Ab 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 Ab1–42-Al (Ab-Al) complex on the gene expression profile of the neuronal-like cell line, SH-SY5Y. Principal Findings: The microarray assay indicated that, compared to Ab or Al alone, exposure to Ab-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 Ca2+ homeostasis as well as in the regulation of glutamatergic transmission and synaptic plasticity. Conclusions and Significance: Ab-Al appears to be largely involved in the molecular machinery that regulates neuronal as well as synaptic dysfunction and loss. Ab-Al seems critical in modulating key AD-related pathways such as glutamatergic transmission, Ca2+ homeostasis, oxidative stress, inflammation, and neuronal apoptosis.
| Titolo: | Microarray analysis on human neuroblastoma cells exposed to aluminum, β(1-42)-amyloid or the β(1-42)-amyloid aluminum complex. |
| Autori: | |
| Data di pubblicazione: | 2011 |
| Rivista: | |
| Abstract: | Background: A typical pathological feature of Alzheimer’s disease (AD) is the appearance in the brain of senile plaques made up of b-amyloid (Ab) 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 Ab 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 Ab1–42-Al (Ab-Al) complex on the gene expression profile of the neuronal-like cell line, SH-SY5Y. Principal Findings: The microarray assay indicated that, compared to Ab or Al alone, exposure to Ab-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 Ca2+ homeostasis as well as in the regulation of glutamatergic transmission and synaptic plasticity. Conclusions and Significance: Ab-Al appears to be largely involved in the molecular machinery that regulates neuronal as well as synaptic dysfunction and loss. Ab-Al seems critical in modulating key AD-related pathways such as glutamatergic transmission, Ca2+ homeostasis, oxidative stress, inflammation, and neuronal apoptosis. |
| Handle: | http://hdl.handle.net/11562/362911 |
| Appare nelle tipologie: | 01.01 Articolo in Rivista |
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| PLos zatta 2011.pdf | Versione dell'editore |  | Open Access Visualizza/Apri |
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