A Transgenic Rat Model of Charcot-Marie-Tooth Disease

نویسندگان

  • Michael Sereda
  • Ian Griffiths
  • Anja Pühlhofer
  • Helen Stewart
  • Moritz J Rossner
  • Frank Zimmermann
  • Josef P Magyar
  • Armin Schneider
  • Ernst Hund
  • Hans-Michael Meinck
  • Ueli Suter
  • Klaus-Armin Nave
چکیده

Charcot-Marie-Tooth disease (CMT) is the most common inherited neuropathy in humans and has been associated with a partial duplication of chromosome 17 (CMT type 1A). We have generated a transgenic rat model of this disease and provide experimental evidence that CMT1A is caused by increased expression of the gene for peripheral myelin protein-22 (PMP22, gas-3). PMP22-transgenic rats develop gait abnormalities caused by a peripheral hypomyelination, Schwann cell hypertrophy (onion bulb formation), and muscle weakness. Reduced nerve conduction velocities closely resemble recordings in human patients with CMT1A. When bred to homozygosity, transgenic animals completely fail to elaborate myelin. We anticipate that the CMT rat model will facilitate the identification of a cellular disease mechanism and serve in the evaluation of potential treatment strategies.

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عنوان ژورنال:
  • Neuron

دوره 16  شماره 

صفحات  -

تاریخ انتشار 1996