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Cited by 182 publications
(154 citation statements)
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References 30 publications
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“…Our results show that prefibrillar ␣Syn oligomers sensitize mitochondria to Ca 2ϩ -induced permeability transition under complex I but not complex II conditions. In light of our findings and existing literature (27,35,58), the most likely explanation for these findings is that ␣Syn acts to inhibit complex I. It has been reported that the brain mitochondria of A53T transgenic mice show reduced complex I activity when compared with wild type (78).…”
Section: Discussionsupporting
confidence: 80%
See 1 more Smart Citation
“…Our results show that prefibrillar ␣Syn oligomers sensitize mitochondria to Ca 2ϩ -induced permeability transition under complex I but not complex II conditions. In light of our findings and existing literature (27,35,58), the most likely explanation for these findings is that ␣Syn acts to inhibit complex I. It has been reported that the brain mitochondria of A53T transgenic mice show reduced complex I activity when compared with wild type (78).…”
Section: Discussionsupporting
confidence: 80%
“…An apparent partial subcellular redistribution of ␣Syn from the cytoplasm to the inner and outer mitochondrial membranes (27,34,35) is correlated with mitochondrial dysfunction, including increased oxidative stress, reduced mitochondrial membrane potential (⌬⌿ m ), altered Ca 2ϩ homeostasis, and cytochrome c release (27, 29 -31, 33, 36, 37). Few studies have directly investigated the effect of different forms of ␣Syn on mitochondrial function.…”
Section: ؉mentioning
confidence: 99%
“…This protective effect is of interest, as α-synuclein is involved in a central pathogenic mechanism for Parkinson disease and has been linked to various aspects of mitochondrial dysfunction (Schapira and Gegg, 2011). Previous studies indicate that the accumulation of α-synuclein in the mitochondria of mammalian dopaminergic neurons leads to reduced mitochondrial complex I activity and increased production of reactive oxygen species (ROS) (Devi et al, 2008;Liu et al, 2009). It is important to note that ROS also act as signaling molecules, and can be involved in a number of pro-survival pathways, including regulation of autophagy (Scherz-Shouval and Elazar, 2007;Weber and Reichert, 2010).…”
Section: Discussionmentioning
confidence: 99%
“…Some studies suggested that α-synuclein can be localized at mitochondria where it inhibits complex I (Devi et al, 2008;Liu et al, 2009;Loeb et al, 2010;Chinta et al, 2010), leading to increased ROS production (Devi et al, 2008;Parihar et al, 2008). Other studies demonstrated increased ROS levels and alterations in the expression levels of complex I subunits due to α-synuclein treatment or over-expression (Pennington et al, 2010;Wang et al, 2010).…”
Section: In Parkinson´s Diseasementioning
confidence: 99%