Charles T. Esmon, Jonathan D. Glass
J Clin Invest.
2009;
119(11):3205–3207
doi:10.1172/JCI40682
This article Copyright © 2009, The American Society for Clinical Investigation
Abstract
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M
utations in the enzyme superoxide dismutase 1 (SOD1) have been linked to the neurodegenerative disease amyotrophic lateral sclerosis (ALS). In this issue of the JCI, Zhong et al. report that the endogenous anticoagulant activated protein C (APC) is able to cross the blood–spinal cord barrier in mice and signal to both neuronal and non-neuronal cells (see the related article beginning on page 3437). This signaling resulted in the suppression of mutant SOD1 synthesis and retarded disease progression in a murine model of ALS. Here we discuss the potential importance of these data and possible relevance to human neurodegenerative diseases.
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