Does laquinimod prevent cuprizone-induced demyelination independent of Toll-like receptor signaling?
Our results confirm that laquinimod prevents demyelination in the cuprizone mouse model for multiple sclerosis via downregulation of NF-κB activation. This laquinimod effect, however, does not involve upstream Toll-like receptor signaling.
Following bilateral DBS for ET, 22% of patients develop a non-disabling dysarthria. Optimal speech outcomes were achieved in 44% of patients and correlated with precise stimulation location within and not outside of the VLp.