Mitochondrial dysfunction associated with increased oxidative stress and α-synuclein accumulation in PARK2 iPSC-derived neurons and postmortem brain tissue

@inproceedings{Imaizumi2012MitochondrialDA,
  title={Mitochondrial dysfunction associated with increased oxidative stress and α-synuclein accumulation in PARK2 iPSC-derived neurons and postmortem brain tissue},
  author={Yoichi Imaizumi and Yohei Okada and Wado Akamatsu and Masato Koike and Naoko Kuzumaki and Hideki Hayakawa and Tomoko Nihira and Tetsuro Kobayashi and Manabu Ohyama and Shigeto Sato and Masashi Takanashi and Manabu Funayama and Akiyoshi Hirayama and Tomoyoshi Soga and Takako Hishiki and Makoto Suematsu and Takuya Yagi and Daisuke Ito and Arifumi Kosakai and K{\^o}z{\^o} Hayashi and Masanobu Shouji and Atsushi Nakanishi and Norihiro Suzuki and Yoshikuni Mizuno and Noboru Mizushima and Masayuki Amagai and Yasuo Uchiyama and Hideki Mochizuki and Nobutaka Hattori and Hideyuki Okano},
  booktitle={Molecular Brain},
  year={2012}
}
Parkinson’s disease (PD) is a neurodegenerative disease characterized by selective degeneration of dopaminergic neurons in the substantia nigra (SN). The familial form of PD, PARK2, is caused by mutations in the parkin gene. parkin-knockout mouse models show some abnormalities, but they do not fully recapitulate the pathophysiology of human PARK2. Here, we… CONTINUE READING