Noted

Alex Eben Meyer

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Research at Yale School of Medicine may point the way to new medications that can alleviate the joint degeneration and pain caused by osteoarthritis, which affects over 30 million people in the US.
     Specialized proteins known as sodium channels, found in cell membranes, produce electrical impulses in “excitable” cells within muscles, the nervous system, and the heart. A sodium channel called Nav1.7 plays a key role in the transmission of pain signals. Researchers found that the same Nav1.7 channels are also present in non-excitable cells that produce collagen and help maintain the joints, and that deleting Nav1.7 genes from these collagen-producing cells significantly reduced joint damage in two osteoarthritis models in mice. They also showed that drugs used to block Nav1.7—including carbamazepine, a treatment for epilepsy and trigeminal neuralgia—gave the mice substantial protection from joint damage.

Using state-of-the-art genomic techniques, plus data from a diverse population, researchers from Yale and the US Department of Veterans Affairs identified hundreds of risk variants located in 22 chromosomal locations significantly associated with cannabis use disorder (CanUD).  
     The researchers note that, given the increasing legalization and public acceptance of cannabis use, examining the genetic basis of CanUD is critical for understanding how it relates genetically to other disorders, and the factors that place some people at higher risk of dependence. Understanding the genetic basis is also crucial for developing effective prevention and treatment strategies.
     The study data also suggested potential causal consequences between cannabis use and lung cancer. Those findings suggest medical and psychiatric public health implications that require further study.