• Frank Zufall, Martina Pyrski, Jan Weiss, and Trese Leinders-Zufall.
• Department of Physiology, University of Saarland School of Medicine, Kirrbergerstrasse 1, Bldg 58, D-66421 Homburg, Germany. frank.zufall@uks.eu
• Arch. Neurol. 2012 Sep 1;69(9):1119-23.

AbstractIn a major breakthrough in our understanding of human olfaction, a recent study showed that loss-of-function mutations in the voltage-gated sodium channel Nav1.7, encoded by the gene SCN9A, cause a loss of the sense of smell (congenital general anosmia) in mice and humans. These findings are of special clinical relevance because Nav1.7 was previously known for its essential role in the perception of pain; therefore, this channel is being explored as a promising target in the search for novel analgesics. This advance offers a functional understanding of a monogenic human disorder that is characterized by a loss of 2 major senses-nociception and smell-thus providing an unexpected mechanistic link between these 2 sensory modalities.

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