Researchers Find New Way to Inhibit Sensory Neuron Growth

Article

In a study published in the Journal of Clinical Investigation, the researchers demonstrated a way to promote sensory neuron growth by blocking a specific molecular signaling pathway.

Researchers at the University of California San Diego School of Medicine, along with colleagues from the National Institute of Diabetes and Digestive and Kidney Diseases, the University of Manitoba and St. Boniface Hospital Albrechtsen Research Centre, have discovered a potential treatment for peripheral neuropathy.

In a study published in the Journal of Clinical Investigation, the researchers demonstrated a way to promote sensory neuron growth by blocking a specific molecular signaling pathway. The blockage also prevented or reversed peripheral neuropathy in cell and rodent models of type 1 and 2 diabetes, chemotherapy-induced neuropathy, and HIV. Muscarinic acetylcholine receptors appear to be responsible for inhibiting the growth of sensory neurons, and a number of antimuscarinic drugs are already on the market.

“This is encouraging because the safety profile of anti-muscarinic drugs is well-characterized, with more than 20 years of clinical application for a variety of indications in Europe,” senior study author Paul Fernyhough, PhD, professor in the departments of pharmacology and therapeutics and physiology at the University of Manitoba, said in a press release. “The novel therapeutic application of anti-muscarinic antagonists suggested by our studies could potentially translate relatively rapidly to clinical use.”

Approximately 20 million Americans are thought to have some form of peripheral neuropathy. It can lead to symptoms such as numbness, muscle weakness, and severe pain.

Reference

Blocking Neuron Signaling Pathway Could Lead to New Treatments for Peripheral Neuropathy [news release]. UCSD’s website. https://health.ucsd.edu/news/releases/Pages/2017-01-17-blocking-neuron-signaling-pathway-could-lead-to-peripheral-neuropathy-treatment.aspx. Accessed Jan. 17, 2017.

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