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- W2079129006 abstract "Abstract Background Calcium (Ca 2+ ) has recently been shown to selectively increase the activity of monoamine oxidase-A (MAO-A), a mitochondria-bound enzyme that generates peroxyradicals as a natural by-product of the deamination of neurotransmitters such as serotonin. It has also been suggested that increased intracellular free Ca 2+ levels as well as MAO-A may be contributing to the oxidative stress associated with Alzheimer disease (AD). Results Incubation with Ca 2+ selectively increases MAO-A enzymatic activity in protein extracts from mouse hippocampal HT-22 cell cultures. Treatment of HT-22 cultures with the Ca 2+ ionophore A23187 also increases MAO-A activity, whereas overexpression of calbindin-D28K (CB-28K), a Ca 2+ -binding protein in brain that is greatly reduced in AD, decreases MAO-A activity. The effects of A23187 and CB-28K are both independent of any change in MAO-A protein or gene expression. The toxicity ( via production of peroxyradicals and/or chromatin condensation) associated with either A23187 or the AD-related β-amyloid peptide, which also increases free intracellular Ca 2+ , is attenuated by MAO-A inhibition in HT-22 cells as well as in primary hippocampal cultures. Conclusion These data suggest that increases in intracellular Ca 2+ availability could contribute to a MAO-A-mediated mechanism with a role in AD-related oxidative stress." @default.
- W2079129006 created "2016-06-24" @default.
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- W2079129006 date "2007-09-16" @default.
- W2079129006 modified "2023-09-27" @default.
- W2079129006 title "Calcium-sensitive regulation of monoamine oxidase-A contributes to the production of peroxyradicals in hippocampal cultures: implications for Alzheimer disease-related pathology" @default.
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- W2079129006 doi "https://doi.org/10.1186/1471-2202-8-73" @default.
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