Mitochondrial hyperpolarization in iPSC-derived neurons from patients of FTDP-17 with 10+16 MAPT mutation leads to oxidative stress and neurodegeneration

Article ID	Journal	Published Year	Pages	File Type
8287212	Redox Biology	2017	13 Pages	PDF

Keywords

2-(N-(7-nitrobenz-2-oxa-1,3-diazol-4-yl)amino)-2-deoxyglucose PSP OXPHOS FTD FCCP ΔΨm IPSC hyperpolarization FTDP-17 CBD IAA VDAC 2-NBDG PDH TMRM PDK hESC ROS iodoacetic acid Alzheimer's disease Oxidative stress Tau Corticobasal degeneration dihydroethidium electron transport chain frontotemporal dementia with Parkinsonism linked to chromosome 17 human embryonic stem cells Induced pluripotent stem cells frontotemporal dementia Oxidative phosphorylation Cerebrospinal fluid CSF tetramethylrhodamine methyl ester Mitochondria DHE ETc Mitochondrial membrane potential Sodium pyruvate pyruvate dehydrogenase Pyruvate dehydrogenase kinase TCA cycle tricarboxylic acid cycle voltage dependent anion channel Carbonyl cyanide-4-(trifluoromethoxy)phenylhydrazone Glycolysis Reactive oxygen species

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Mitochondrial hyperpolarization in iPSC-derived neurons from patients of FTDP-17 with 10+16 MAPT mutation leads to oxidative stress and neurodegeneration

Authors

NoemÃ Esteras, Jonathan D. Rohrer, John Hardy, Selina Wray, Andrey Y. Abramov,