2020
DOI: 10.1016/j.mad.2020.111385
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Mitochondria and cellular redox state on the route from ageing to Alzheimer’s disease

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Cited by 31 publications
(18 citation statements)
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“…Chronic systemic OxS stimulates a cascade of reactive oxygen species (ROS) and reactive nitrogen species (RNS), which impairs the blood–brain barrier (BBB), and contributes to lipid peroxidation, oxidation of proteins and nucleic acids, brain cell damage, and even cell death. Nevertheless, a thin line separates the harmful from beneficial ROS effects, depending on redox balance: they not only act as damaging agents, but also participate in cellular signaling and regulation [ 9 ]. In fact, polyphenol benefits have been partly attributed to their pro-oxidant activities [ 10 , 11 ].…”
Section: Introductionmentioning
confidence: 99%
“…Chronic systemic OxS stimulates a cascade of reactive oxygen species (ROS) and reactive nitrogen species (RNS), which impairs the blood–brain barrier (BBB), and contributes to lipid peroxidation, oxidation of proteins and nucleic acids, brain cell damage, and even cell death. Nevertheless, a thin line separates the harmful from beneficial ROS effects, depending on redox balance: they not only act as damaging agents, but also participate in cellular signaling and regulation [ 9 ]. In fact, polyphenol benefits have been partly attributed to their pro-oxidant activities [ 10 , 11 ].…”
Section: Introductionmentioning
confidence: 99%
“…However, others have observed the beneficial effects of ROS on mitochondria and in various cellular pathways [38,39]. Low levels of ROS are shown to have beneficial effects while high levels of ROS are associated with AD, suggesting a threshold determines whether ROS is beneficial or harmful [40]. The low levels of ROS regulate various cellular pathways, such as H 2 O 2 regulating various signaling pathways with proteins containing cysteine residues [41].…”
Section: Figurementioning
confidence: 99%
“…Mitochondrial ETC dysfunction was already described in several cellular and transgenic mouse models of AD [ 43 , 45 , 46 ]. However, it is worth considering that Cu-exposure additionally exacerbates the activity of several proteins associated with the mitochondrial ETC complexes ( Table 1 and Figure 2 ).…”
Section: Mitochondrial Proteome Altered Upon Copper Exposure In Ad Identified By Proteomics Approachesmentioning
confidence: 99%