Inhibition of Drp1 Ameliorates Synaptic Depression, Aβ Deposition, and Cognitive Impairment in an Alzheimer's Disease Model.

@article{Baek2017InhibitionOD,
  title={Inhibition of Drp1 Ameliorates Synaptic Depression, Aβ Deposition, and Cognitive Impairment in an Alzheimer's Disease Model.},
  author={Seung Hyun Baek and So Jung Park and Jae In Jeong and Sung Hyun Kim and Jihoon Han and Jae Won Kyung and Sang-Ha Baik and Yuri Choi and Bo Youn Choi and Jin Su Park and Gahee Bahn and Ji Hyun Shin and Doo Sin Jo and Joo-Yong Lee and C G Jang and Thiruma Valavan Arumugam and Jongpil Kim and Jeung-Whan Han and Jae-Young Koh and Dong-Hyung Cho and D H Jo},
  journal={The Journal of neuroscience : the official journal of the Society for Neuroscience},
  year={2017},
  volume={37 20},
  pages={5099-5110}
}
Excessive mitochondrial fission is a prominent early event and contributes to mitochondrial dysfunction, synaptic failure, and neuronal cell death in the progression of Alzheimer's disease (AD). However, it remains to be determined whether inhibition of excessive mitochondrial fission is beneficial in mammal models of AD. To determine whether dynamin-related protein 1 (Drp1), a key regulator of mitochondrial fragmentation, can be a disease-modifying therapeutic target for AD, we examined the… CONTINUE READING
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