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The Wld S gene modestly prolongs survival in the SOD1 G93A fALS mouse
Journal article   Open access   Peer reviewed

The Wld S gene modestly prolongs survival in the SOD1 G93A fALS mouse

Lindsey R. Fischer, Deborah G. Culver, Albert A. Davis, Philip Tennant, Minsheng Wang, Michael Coleman, Seneshaw Asress, Robert Adalbert, Guillermo M. Alexander and Jonathan D. Glass
Neurobiology of disease, v 19(1), pp 293-300
2005
url
https://doaj.org/article/13be9544346a497092844024b6a267f8View
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Abstract

ALS Amyotrophic lateral sclerosis Axonal degeneration SOD1 Wallerian degeneration WldS
The “slow Wallerian degeneration” ( Wld S ) gene is neuroprotective in numerous models of axonal degeneration. Axonal degeneration is an early feature of disease progression in the SOD1 G93A mouse, a widely used model of familial amyotrophic lateral sclerosis (fALS). We crossed the Wld S mouse with the SOD1 G93A mouse to investigate whether the Wld S gene could prolong survival and modify neuropathology in these mice. SOD/ Wld S mice showed levels of motor axon loss similar to that seen in SOD1 G93A mice. The presence of the Wld S gene, however, modestly prolonged survival and delayed denervation at the neuromuscular junction. Prolonged survival was more prominent in female mice and did not depend on whether animals were heterozygous or homozygous for the Wld S gene. We also report that SOD1 G93A mice show significant degeneration of sensory axons during the course of disease, supporting previous data from humans demonstrating that ALS is not purely a motor disorder.

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