[HTML][HTML] Activated protein C therapy slows ALS-like disease in mice by transcriptionally inhibiting SOD1 in motor neurons and microglia cells
Z Zhong, H Ilieva, L Hallagan, R Bell… - The Journal of …, 2009 - Am Soc Clin Investig
The Journal of clinical investigation, 2009•Am Soc Clin Investig
Mutations 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 …
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 …
Mutations 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.
The Journal of Clinical Investigation