Early detachment of neuromuscular junction proteins in ALS mice with SODG93A mutation

@inproceedings{Narai2009EarlyDO,
  title={Early detachment of neuromuscular junction proteins in ALS mice with SODG93A mutation},
  author={Hisashi Narai and Yasuhiro Manabe and Makiko Nagai and Isao Nagano and Yasuyuki Ohta and Toshikazu Murakami and Yasushi Takehisa and Tatsushi Kamiya and Koji Abe},
  booktitle={Neurology international},
  year={2009}
}
The transgenic animals with mutant copper/zinc superoxide dismutase (SOD1) DNA develop paralytic motor neuron disease resembling human amyotrophic lateral sclerosis (ALS) patients and are commonly used as models for ALS. In the transgenic (Tg) mice with the G93A mutation of the human SOD1 gene SOD1(G93A) mice), the loss of ventral root axons and the synapses between the muscles and the motor neurons suggested that the motor neuron degeneration might proceed in a dying-back degeneration pattern… CONTINUE READING

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