. ATF3 expression improves motor function in the ALS mouse model by promoting motor neuron survival and retaining muscle innervation. Proc Natl Acad Sci U S A. 2014 Jan 28;111(4):1622-7. Epub 2014 Jan 13 PubMed.

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  1. This is an interesting manuscript. The authors demonstrated that transgenic overexpression of ATF3 in motor neurons of SOD1 mice promoted motor neuron survival and maintained axonal integrity and neuromuscular junction (NMJ) innervations. They found in ATF3/SOD1 mice compared to SOD1 transgenic that a) motor neuron survival was higher, b) there was a reduction in the percentage of large-caliber axons and an increase in the percentage of small-caliber axons, c) the percentage of NMJ innervations was higher, d) muscle atrophy was decreased, and e) ATF3 overexpression slowed onset of disease and slightly prolonged survival (by 7.7 days). ATF3 expression alone was not sufficient to halt disease progression. Importantly, ATF3 overexpression only slowed loss of grip strength by about 10 days. Thus, the nascent collaterally innervated NMJs appear to inhibit muscle atrophy but do not sufficiently maintain muscle strength. Increasing ATF3 expression is an interesting approach to promote motor neuron survival and axonal growth but will likely need to be coupled with other therapeutics to slow/halt the progression of ALS and improve muscle function in patients.

    View all comments by Jeffrey Jasper

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