Oxidative stress and altered mitochondrial protein expression in the absence of amyloid-β and tau pathology in iPSC-derived neurons from sporadic Alzheimer's disease patients.

@article{Birnbaum2018OxidativeSA,
  title={Oxidative stress and altered mitochondrial protein expression in the absence of amyloid-β and tau pathology in iPSC-derived neurons from sporadic Alzheimer's disease patients.},
  author={Julian H Birnbaum and Debora Wanner and A. F. Gietl and Antje Saake and Thomas M. K{\"u}ndig and C. Hock and Roger M. Nitsch and Christian Tackenberg},
  journal={Stem cell research},
  year={2018},
  volume={27},
  pages={
          121-130
        }
}
Mitochondrial dysfunction is a prominent feature of Alzheimer's disease (AD) and increased production of reactive oxygen species (ROS) has been described in postmortem brain samples and animal models. However, these observations were made at a late stage of disease and the inability to examine an early, presymptomatic phase in human neurons impeded our understanding of cause or consequence of mitochondrial dysfunction in AD. We used human induced pluripotent stem cell-derived neuronal cells (iN… CONTINUE READING
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